Pain Procedures in Clinical Practice: Expert Consult: Online and Print

PAIN PROCEDURES in CLINICAL PRACTICE 3RD EDITION

Ted A. Lennard, MD Clinical Assistant Professor Department of Physical Medicine and Rehabilitation University of Arkansas Little Rock, Arkansas Springfield Neurological and Spine Institute Cox Health Systems Springfield, Missouri

Stevan Walkowski, DO Ohio University College of Osteopathic Medicine Athens, Ohio

Aneesh K. Singla, MD, MPH Instructor Harvard Medical School Department of Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts

David G. Vivian, MM, BS, FAFMM Medical Director Metro Pain Clinics Metro Spinal Clinic Clinical Intelligence Victoria, Australia



1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

ISBN: 978-1-4160-3779-8

PAIN PROCEDURES IN CLINICAL PRACTICE Copyright © 2011, 2000 by Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without ­permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Pain procedures in clinical practice / Ted A. Lennard … [et al.]. -- 3rd ed. p. ; cm. Includes bibliographical references and index. ISBN 978-1-4160-3779-8 (hardcover : alk. paper) 1. Medicine, Physical. 2. Medical rehabilitation. I. Lennard, Ted A., 1961[DNLM: 1. Pain—therapy. 2. Pain—prevention & control. 3. Rehabilitation—methods. WL 704] RM700.P46 2011 616’.0472—dc22 2011004326

Acquisitions Editor: Daniel Pepper Senior Developmental Editor: Deidre Simpson Publishing Services Manager: Patricia Tannian Team Manager: Radhika Pallamparthy Senior Project Manager: Sharon Corell Project Manager: Joanna Dhanabalan Design Direction: Louis Forgione

Printed in China Last digit is the print number:  9  8  7  6  5  4  3  2  1 

To my wife, Suzanne, and our four daughters, Selby, Claire, Julia, and Maura. Ted A. Lennard

TRIBUTE We were saddened to hear of the death of Jay Govind, MBChB, DPH, MMed, FAFOM, on June 20, 2009. Dr. Govind was extensively involved in the content of the “Spine” section of this edition. He served in many capacities throughout his professional career, most recently as the senior specialist and director of the Pain Management Unit at Canberra Hospital. He was the past president of The Australian Faculty of Musculoskeletal Medicine. He also was a board member of the International Spinal Intervention Society and served as chairman of the Standards Committee. Dr. Govind lectured extensively and had a special interest in neck and back pain. He made a significant contribution to pain services, influenced attitudes toward pain, and brought new ideas to the management of chronic pain. He was a prolific writer, clinician, researcher, teacher, and a compassionate and kind man. We were also saddened to learn of the death of Peter Huijbregts, PT, MSc, MHSc, DPT, OCS, FAAOMPT, FCAMT, on November 6, 2010. Dr. ­Huijbregts enthusiastically accepted the task of authoring the chapter on “Manual Therapy.” His passion and expertise were in the field of orthopedic and manual physical therapy. He wrote many book chapters and research papers and co-authored many texts. Dr. Huijbregts practiced in Victoria, British-Columbia, Canada, but was originally trained in The Netherlands. He completed two separate research master’s degrees and a doctorate in physical therapy. He was well known for his generosity, sense of humor, and humility. Each of these men will be missed by all who knew them. Ted A. Lennard, MD

vii

Contributors

Shihab Ahmed, MD, MPH

Medical Director Massachusetts General Hospital Pain Clinic Lowell General Hospital Lowell, Massachusetts Emerson Hospital Concord, Massachusetts

Steven T. Akeson, PsyD

Neuropsychological Association of Southwest Missouri, PC Springfield, Missouri

Alvin K. Antony, MD FABPMR

Director Physical Medicine and Rehabilitation Carolina Sports and Spine, PA Rocky Mount, North Carolina

Charles N. Aprill, MD

Interventional Spine Specialists Kenner, Louisiana

Robert Baker, DO

Resident PGY-1 New York College of Osteopathic Medicine Department of Osteopathic Manipulative Medicine St. Barnabas Hospital Bronx, New York

Joel Jay Baumgartner, MD

CAQ Sports Medicine, Rejuv Medical Sartell, Minnesota

William Jeremy Beckworth, MD

James MackIntosh Borowczyk, BSc, MB, ChB, MMed (Pain), DMM, FRCP (Edin), FAFMM Musculoskeletal Medicine Senior Clinical Lecturer Academic Coordinator of Postgraduate Musculoskeletal and Pain Studies Department of Orthopaedics and Musculoskeletal Medicine University of Otago Christchurch School of Medicine and Health Sciences Senior Clinical Lecturer Department of Orthopaedics and Musculoskeletal Medicine Christchurch Hospital Christchurch, New Zealand

Kenneth Botwin, MD Fellowship Director Florida Spine Institute Clearwater, Florida

Gerry Catapang, PT, DPT, MGS

Physical Therapy Care Manual Physical Therapy and Industrial Rehabilitation Center, PC Springfield, Missouri

Lalaine Madlansacay Catapang, PT

Physical Therapy Care Manual Physical Therapy and Industrial Rehabilitation Center, PC Springfield, Missouri

Philip Ceraulo, DO

Florida Spine Institute Clearwater, Florida

Assistant Professor Department of Physical Medicine and Rehabilitation and Orthopedics Emory University Atlanta, Georgia

SriKrishna Chandran, MD

William M. Boggs, MD

President Republic Physical Therapy Republic, Missouri

Center for Clinical Trials Research University of Florida, College of Medicine Micanopy, Florida

Department of Physical Medicine and Rehabilitation Johns Hopkins Bayview Medical Center Baltimore, Maryland

Peter M. Chanliongco, PT

Martin K. Childers, DO, PhD

Professor Neurology Wake Forest Institute for Regenerative Medicine Winston-Salem, North Carolina ix

x  Contributors

Marissa H. Cohler, MD

Resident Physician Physical Medicine and Rehabilitation Rehabilitation Institute of Chicago, Northwestern University ­Feinberg School of Medicine Chicago, Illinois

William F. Craig

Physiatrist Physical Medicine and Rehabilitation Southlake Orthopaedics Birmingham, Alabama

Susan J. Dreyer, MD

Associate Professor Orthopaedic Surgery and Physical Medicine and Rehabilitation Emory University School of Medicine Emory University Hospital Atlanta, Georgia

Steve R. Geiringer, MD

Clinical Professor Physical Medicine and Rehabilitation Wayne State University Detroit, Michigan

Herman C. Gore, MD

Fellow Georgia Pain Physicians, PC Marietta, Georgia; Forest Park, Georgia; Calhoun, Georgia

Padma Gulur, MD

Instructor Anesthesia Harvard Medical School Director, Inpatient Pain Service Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts

Linda Lingzhi Hao, DOM, PhD

Vice President International Academy of Scalp Acupuncture Santa Fe, New Mexico

Danielle R. Hathcock, MS

Neuropsychological Association of Southwest Missouri, PC Springfield, Missouri

Jodi J. Hawes, MD, PT

Duke University Hospital Durham, North Carolina

Peter A. Huijbregts, PT, MSc, MHSc, DPT, OCS, FAAOMPT, FCAMT Shelbourne Physiotherapy Clinic Victoria, British Columbia, Canada

Rodney Jones, MD

Clinical Assistant Professor Anesthesiology University of Kansas School of Medicine-Wichita Active Staff Anesthesiology HCA-Wesley Via-Christi Hospitals Vice President Kansas Spine Institute, LLC Wichita, Kansas

Jatin Joshi, MD

Massachusetts General Hospital Boston, Massachusetts

Wade King, MB, BS, MMedSc, MMed (Med), DMM, FAFMM

Assistant Professor Neurology, Section of Physical Medicine and Rehabilitation Wake Forest University School of Medicine Winston-Salem, North Carolina

Research Fellow Department of Clinical Research University of Newcastle Visiting Medical Officer in Interventional Pain Medicine Royal Newcastle Centre Visiting Medical Officer in Pain Management Pendlebury Clinic Private Hospital Newcastle, New South Wales, Australia Associate Lecturer Department of Orthopaedics and Musculoskeletal Medicine University of Otago Christchurch, New Zealand

Dale A. Halfaker, PhD

Milton H. Landers, DO, PhD

Hongtao Michael Guo, MD, PhD

Neuropsychological Association of Southwest Missouri, PC Springfield, Missouri

Daniel E. Halpert, DO

Resident Physical Medicine and Rehabilitation Johns Hopkins University School of Medicine Baltimore, Maryland

Jason Jishun Hao, DOM, MTCM, MBA

President International Academy of Scalp Acupuncture Santa Fe, New Mexico

Associate Clinical Professor Department of Anesthesiology University of Kansas, School of Medicine-Wichita Medical Director Kansas Spine Institute Wichita, Kansas

Ted A. Lennard, MD

Clinical Assistant Professor Department of Physical Medicine and Rehabilitation University of Arkansas Little Rock, Arkansas Springfield Neurological and Spine Institute Cox Health Systems Springfield, Missouri

Contributors  xi

Michael S. Leong, MD

Clinical Assistant Professor Clinic Chief Anesthesia Stanford Pain Management Center Redwood City, California Stanford University Medical Center Stanford University Palo Alto, California

Karan Madan, MBBS, MPH

Instructor in Anesthesia Department of Anesthesia, Pain, and Perioperative Medicine Harvard University Associate Clinical Director Department of Anesthesia, Pain, and Peroperative Medicine Brigham and Women’s Hospital Boston, Massachusetts

Jeffrey J. Patterson, DO

Professor, Emeritis Department of Family Medicine University of Wisconsin School of Medicine and Public Health Madison, Wisconsin

Jeffrey D. Petersohn, MD

Adjunct Associate Professor Department of Anesthesiology Drexel University School of Medicine Philadelphia, Pennsylvania PainCare, PC Linwood, New Jersey

Kim Pollock, RN, MBA, CPC

Consultant Karen Zupko and Associates, Inc Chicago, Illinois

Aram Mardian, MD

Joel M. Press, MD

Curtis Mattson, MS

Elmer G. Pinzon, MD

Maricopa County Hospital Phoenix, Arizona Neuropsychological Association of Southwest Missouri, PC Springfield, Missouri

Timothy P. Maus, MD

Assistant Professor of Radiology Mayo Clinic Rochester, Minnesota

Bruce Mitchell, MM, BS, FACSP Metro Spinal Clinic Caulfield South Victoria, Australia

Alex Moroz, MD, FACP

Director of Medical Education and Residency Training Rehabilitation Medicine New York University School of Medicine Director of Integrative Musculoskeletal Medicine Program Director of Musculoskeletal Rehabilitation Unit Rusk Institute of Rehabilitation Medicine Adjunct Professor Tri-State College of Acupuncture New York, New York

Susan M. Donnelly Murphy, JD Massachusetts Bar Association Murphy and Riley, PC Boston, Massachusetts

Jordan L. Newmark, MD

Clinical Fellow in Anesthesia Department of Anesthesia Harvard Medical School Anesthesia Resident-Physician Department of Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts

Nicholas K. Olsen, DO

Clinical Instructor Physical Medicine and Rehabilitation University of Colorado at Denver and Health Sciences Center Thornton, Colorado

Center for Spine, Sports, and Occupational Rehabilitation Chicago, Illinois Fellow Georgia Pain Physicians, PC Marietta, Georgia; Forest Park, Georgia; Calhoun, Georgia

David Rabago, MD

University of Wisconsin School of Medicine and Public Health Department of Family Medicine Madison, Wisconsin

Albert C. Recio, MD, RPT, PTRP

Assistant Professor Department of Physical Medicine and Rehabilitation Johns Hopkins University, School of Medicine Medical Director of Aquatic Therapy The International Center for Spinal Cord Injury Kennedy Krieger Institute Baltimore, Maryland

Steven H. Richeimer, MD

Chief Division of Pain Medicine Associate Professor Department of Anesthesiology Keck School of Medicine, University of Southern California Los Angeles, California

Anna C. Schneider, BS

Coordinator for Faculty Research The International Center for Spinal Cord Injury Kennedy Krieger Institute Baltimore, Maryland

Robert A. Schulman, MD

Physical Medicine, Rehabilitation, Medical Acupuncture, and Electrodiagnostic Medicine New York, New York

Joel D. Sebag, DPT

Doctor of Physical Therapy, Physical Therapist, and CEO Mountaincrest Rehabilitation Services Harrison, Arkansas

xii  Contributors

Chunilal P. Shah, MD, MBBS, BS

Stevan Walkowski, DO

C. Norman Shealy, MD, PhD

Ajay D. Wasan, MD, MSc

Florida Spine Institute Clearwater, Florida

Professor Emeritus of Energy Medicine Holos University Graduate Seminary Bolivar, Missouri President Holos Institutes of Health, Inc Fair Grove, Missouri

Julie K. Silver, MD

Ohio University College of Osteopathic Medicine Athens Ohio Assistant Professor Anesthesiology and Psychiatry Harvard Medical School Brigham and Women’s Hospital Boston, Massachusetts

Robert E. Windsor, MD, FAAPMR, FAAEM, FASPM

Assistant Professor Department of Physical Medicine and Rehabilitation Harvard Medical School Boston, Massachusetts

Assistant Clinical Professor Emory University Department of Physical Medicine and Rehabilitation President, Georgia Pain Physicians, PC Marietta, Georgia; Forest Park, Georgia; Calhoun, Georgia

Aneesh K. Singla, MD, MPH

Ted L. Wunderlich, BA

Instructor Harvard Medical School Department of Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts

Fereshteh Sharonah Soumekh, MD

Clinical Instructor, Neurology Harvard Medical School Co-Director Pain Clinic Neurology Boston Veterans Administration Healthcare System Neurology Consultant Anesthesiology Brigham and Women’s Hospital Boston, Massachusetts

Peter Stefanovich, MD

Instructor Harvard Medical School Attending Anesthesiologist Anesthesia, Critical Care, and Pain Management Massachusetts General Hospital Boston, Massachusetts

David G. Vivian, MM, BS, FAFMM Medical Director Metro Pain Clinics Metro Spinal Clinic Clinical Intelligence Victoria, Australia

Brian J. Wainger, MD, PhD

Department of Anesthesia Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts

Neuropsychological Association of Southwest Missouri, PC Springfield, Missouri

Eric Yarnell, ND

Associate Professor Botanical Medicine Bastyr University Kenmore, Washington

Ahn Young, MD

Massachusetts General Hospital Boston, Massachusetts

Jeffrey L. Young, MD

Physicians Review Network of New York New York, New York

Andrea H. Zengion, ND, MSAOM

Naturopathic Doctor and Acupuncturist San Francisco Natural Medicine San Francisco, California

Yi Zhang, MD, PhD, MSc

Instructor Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital, Harvard Medical School Boston, Massachusetts

Li Zhang, MD, PhD

Department of Anesthesiology Columbia University Medical Center New York, New York

Preface

The diagnosis and treatment of pain-related conditions have changed extensively over the last decade. These changes have included surgical advances in minimally invasive techniques, multidisciplinary approaches to complex pain problems, the development of numerous oral and injectable medications, and further advancements in pain management injection procedures. Our understanding of many of these changes has been advanced by our own specialty academies and many new societies dedicated to pain relief. These groups have been instrumental in encouraging research that has been included in much of this edition of Pain Procedures in Clinical Practice. The third edition of Pain Procedures in Clinical Practice has changed extensively since the original volume was published in 1995. The original text was directed toward practicing physiatrists and incorporated inpatient rehabilitation and outpatient pain management procedures. In 2000 the second edition was expanded as a multi-specialty textbook and intended entirely for the pain

management practitioner, regardless of medical specialty. The third edition of Pain Procedures in Clinical Practice has been further expanded to include section editors. The extensive volume of new information, research, and techniques relative to pain management necessitated this expansion. The selected section editors are well known in their respective specialities. To each of them—Dr. ­Stevan Walkowski (CAM Procedures), Dr. Aneesh Singla (Peripheral Nerve Blocks), Dr. David Vivian (Spine Procedures), and Dr. ­Steven Richiemer (Video Procedures)—I extend my gratitude for their hard work and dedication to this textbook. A huge thank-you goes out to all of the authors for contributing their expertise to this text. Numerous hours of research, writing, and review were required by each of these contributors to produce such a volume. In addition, special thanks go out to the publisher and medical artists who made this project come to fruition. Ted A. Lennard, MD Editor

xiii

Fundamentals of Procedural Care

1

Ted A. Lennard, MD

Pain procedures are a useful adjunct in managing pain and functional problems. The pain physician, as a diagnostician, can derive valuable information from the results of these procedures and from patient responses. This information can be invaluable in directing future treatment. Knowledge of the fundamentals of procedural care is important to novices and experienced physicians who provide such treatment to reduce complications, eliminate unnecessary procedures, and maximize patient recovery.

Procedure Planning The patient work-up should begin with a detailed history and a physical examination that focuses on the body part involved. Historical emphasis on the duration of symptoms, previous attempts at procedures, and pending litigation should be well documented. Signs of symptoms magnification and malingering should be noted.1,2 A thorough functional, social, and psychological history should be included. A comparison of historical and physical findings with available imaging studies is essential to complete the evaluation. During the evaluation period, diagnostic procedures can be useful in providing valuable insight into the patient’s pain generator, anatomic defect, threshold for pain, and psychological response to treatment. When a provisional diagnosis is made, treatment objectives should be outlined. Conservative, nonprocedural-oriented treatment should be undertaken initially if symptoms are not disabling. This treatment should include correction of underlying biomechanical disorders, activity modification in the workplace, technique changes in athletes, and flexibility and strengthening programs. Concomitant psychological disorders also should be treated. Upon deciding to proceed with a therapeutic procedure, the physician should be certain it is performed within the context of a welldesigned rehabilitation program.

General Procedure Techniques Positioning and Relaxation Positioning the patient for comfort and physician accessibility is an important step in good technique. Multiple pillows, foam plinths, and pads can be used to increase the patient’s tolerance on hard procedure tables, provide some degree of relaxation, and optimize positioning. This is especially important for the patient with cardiac or pulmonary compromise. For the physician, chairs and procedure

tables for proper height prevent fatigue during lengthy procedures and improve manual dexterity. Constant communication with the patient, including explanations of approaching procedural steps, helps reduce anxiety. Inappropriate conversation with assisting medical personnel should be avoided, thereby confirming the physician’s total attention to the patient. The patient’s gown should fit properly, enhancing relaxation and comfort. If these techniques do not lead to relaxation, oral or parenteral sedation should be provided. Skin Preparation Because skin cannot be sterilized without damage, the goal of antiseptics is to remove transient and pathogenic microorganisms while reducing resident flora to a low level.3 These agents should be safe, rapid-acting, inexpensive, and effective on a broad spectrum of organisms.3,4 Multiple agents, including iodophors (Betadine), hexachlorophene (pHisoHex), chlorhexidine (Hibiclens, Hibitane), and alcohols, are commercially available and accomplish these desired goals.3,5-7 The preferred agent remains controversial.3,8-13 Clinically, the most commonly used agents are alcohol and iodine, with the latter being superior for skin decontamination.16 Application of 70% isopropyl alcohol destroys 90% of the cutaneous bacteria in 2 minutes, whereas the usual single wipe without waiting procedure destroys, at most, 75% of cutaneous bacteria.3 Skin regions with hair should not alter one’s method of skin decontamination. Hair removal by shaving increases wound infection rate and is contraindicated.17-19 If absolutely necessary, clipping hair20,21 or applying depilatory creams19 can be safe.22 The overall risk of wound infection with most pain procedures is low and mostly depends on the technique that the practitioner employs during the procedure.

Needle Insertion and Local Anesthesia Steps should be taken to make all procedures as pain-free as possible. The liberal use of local anesthetics in adequate concentrations will promote this goal while minimizing repeat needle sticks. Small diameter needles, 28 to 30 gauge, are initially used to anesthetize the skin and subcutaneous tissue. Distracting the skin with one’s fingers while slowly advancing the needle helps to reduce pain. The tip of the needle can be placed in the subcutaneous fat and, upon injection, less pain is noted than with intradermal injections because of the distensibility of fat. Rapid infusion of medication, especially with large volumes, causes tissue distention and 3

4  Basic Principles of Procedures

results in pain. Lidocaine23-26 and bupivacaine,27 buffered with 8.4% sodium bicarbonate causes less pain than plain anesthetics and is equally efficacious. A 1:10 to 1:20 ratio of sodium bicarbonate to anesthetics can be used. Morris and colleagues found that, when injected, subcutaneous procaine and lidocaine were the least painful anesthetics.28,29 Only etidocaine was found to be more painful than bupivacaine. Varelmann and coworkers found that patients who were told “We are going to give you a local anesthetic that will numb the area and you will be comfortable during the procedure” perceived less pain than patients who were told “You are going to feel a big bee sting; this is the worst part of the procedure.”30 Other preparations used to reduce pain with initial needle injections include topical anesthetics (eutectic mixtures of local anesthetics, or EMLA), vapocoolant sprays, and preheated local anesthetics.31 If the patient is intolerant of or allergic to anesthetic agents, 0.9% intradermal saline or dilute antihistamines such as diphenhydramine (Benadryl) in 10 to 25 mg/mL injections can be used as alternatives;32 however, they are often considered painful, especially when injected intradermally. Before administering injection anesthetics, one should aspirate to prevent inadvertent injection into a vascular structure. Smallgauge needles are unreliable when aspirating for blood. Needles of 25 gauge or larger rotated in two planes are necessary for this purpose. Continual movement of the needle tip makes injection into a vessel less likely. Slow, fractionated dosing is recommended while monitoring the patient for early signs of anesthetic toxicity.

Precautions Good technique not only reduces the risk of wound infection, but also lowers the rate of viral transmission between patient and physician. Physicians who perform exposure-prone procedures should know their own human immunodeficiency virus (HIV) and hepatitis B virus (HBV) antibody status. The risk to the patient of contracting the HIV virus ranges from 1 in 42,000 to 1 in 420,000; the risk of contracting fatal HBV infection from an HBeAg positive surgeon during a procedure ranges from 1 in 76,000 to 1 in 1.4  ­million.33 Universal precautions should be understood and include the use of gloves, protective eyewear, masks, (optional), and gowns (optional). Recapping used needles should be avoided and is seldom necessary. REFERENCES   1. Becker GE. Red Flags. Oakland, Calif: American Back Society Newsletter; 1991, p 23.   2. Carragee EJ. Psychological and functional profiles in select subjects with low back pain. Spine J. 2001;1(3):198-204.   3 Sebben JE. Surgical antiseptics. J Am Acad Dermatol. 1983;9:759-765.   4. Masterson BJ. Skin preparation. Clin Obstet Gynecol. 1988;31:736-743.   5. Davies J, Babb JR, Ayliffe GA, Wilkins MD. Disinfection of skin of the abdomen. Br J Surg. 1979;65:855-858.   6. Lepor NE, Madyoon H. Antiseptic skin agents for percutaneous procedures. Rev Cardiovasc Med. 2009;10(4):187-193.   7. Ritter MA, French ML, Eitzen HE, et al. The antimicrobial effectiveness of operative-site preparative agents: a microbiological and clinical study. J Bone Joint Surg Am. 1980;62:826-828.   8. Bibbo C, Patel DV, Gehrmann RM, Lin SS. Chlorhexidine provides superior skin decontamination in foot and ankle surgery: A prospective randomized study. Clin Orthop Relat Res. 2005;438:204-208.   9. Calfee DP, Farr BM. Comparison of four antiseptic preparations for skin in the prevention of contamination of percutaneously drawn blood ­cultures: A randomized trial. J Clin Microbiol. 2002;40(5):1660-1665.

10. Kiyoyama T, Tokuda Y, Shiiki S, et al. Isopropyl alcohol compared with isopropyl alcohol plus povidone-iodine as skin preparation for prevention of blood culture contamination. J Clin Microbiol. 2009;47(1):54-58. 11. Lowbury EJ, Lilly HA. Use of 4% chlorhexidine detergent solution (Hibiscrub) and other methods of skin disinfection. Br Med J. 1973;1:510-515. 12. Saltzman MD, Nuber GW, Gryzlo SM, et al. Efficacy of surgical preparation solutions in shoulder surgery. J Bone Joint Surg Am. 2009 Aug;91(8):1949-1953. 13. Smylie HG, Logie JR, Smith G. From Phisohex to Hibiscrub. Br Med J. 1973;4:586-589. 14. Swenson BR, Hedrick TL, Metzger R, et al. Effects of preoperative skin preparation on postoperative wound infection rates: A prospective study of 3 skin preparation protocols. Infect Control Hosp Epidemiol. 2009 Oct;30(10):964-971. 15. Tunevall TG. Procedures and experiences with preoperative skin preparation in Sweden. J Hosp Infect. 1988;11 (suppl B):11-14. 16. Choudhuri M, McQueen R, Inoue S, et al. Efficiency of skin sterilization for a venipuncture with the use of commercially available alcohol or iodine pads. Am J Infect Control. 1990;18:82-85. 17. Bird BJ, Chrisp DB, Scrimgeour G. Extensive pre-operative shaving: A costly exercise. N Z Med J. 1984;97:727-729. 18. Celik SE, Kara A. Does shaving the incision site increase the infection rate after spinal surgery? Spine. 2007;32(15):1575-1577. 19. Seropian R, Reynolds BM. Wound infections after preoperative depilatory versus razor preparation. Am J Surg. 1971;121:251-254. 20. Mackenzie I. Preoperative skin preparation and surgical outcome. J Hosp Infect. 1988;11:27-32. 21. Olson MM, MacCallum J, McQuarrie DG. Preoperative hair removal with clippers does not increase infection rate in clean surgical wounds. Surg Gynecol Obstet. 1986;162:181-182. 22. Tanner J, Moncaster K, Woodings D. Preoperative hair removal: A systematic review. J Perioper Pract. 2007;17(3):118-121, 124-132. 23. McKay W, Morris R, Mushlin P. Sodium bicarbonate attenuates pain on skin infiltration with lidocaine, with or without epinephrine. Anesth Analg. 1987;66:572-574. 24. Roberts JR. Local anesthetics: Injection techniques. Emerg Med News. 1992 March;9-16. 25. Stewart JH, Chinn SE, Cole GW, et al. Neutralized lidocaine with ­epinephrine for local anesthesia – II. J Dermatol Surg Oncol. 1990;16: 842-845. 26. Xia Y, Chen E, Tibbits DL, et al. Comparison of effects of lidocaine hydrochloride, buffered lidocaine, diphenhydramine, and normal saline after intradermal injection. J Clin Anesth. 2002;14(5):339-343. 27. Cheney PR. Molzen G, Tandberg D: The effect of pH buffering on reducing the pain associated with subcutaneous infiltration of bupivicaine. Am J Emerg Med. 1991;9:147-148. 28. Morris R, McKay W, Mushlin P. Comparison of pain associated with intradermal and subcutaneous infiltration with various local anesthetic solutions. Anesth Analg. 1987;66:1180-1182. 29. Morris RW, Whish DK. A controlled trial of pain on skin infiltration with local anaesthetics. Anaesth Intensive Care. 1984;12:113-114. 30. Varelmann D, Pancaro C, Cappiello EC, Camann WR. Noceboinduced hyperalgesia during local anesthetic injection. Anesth Analg. 2010;110(3):868-870. 31. Bloom LH, Scheie HG, Yanoff M. The warming of local anesthetic agents to decrase discomfort. Ophthalmic Surg. 1984;15:603. 32. Mark LC. Avoiding the pain of venipuncture (letter to the editor). N Engl J Med. 1976;294:614. 33. Lo B, Steinbrook R. Health care workers infected with the human immunodeficiency virus. The next steps. JAMA. 1992;267:1100-1105.

Commonly Used Medications in Procedures

2

Susan J. Dreyer, MD, and William Jeremy Beckworth, MD

Local anesthetics, corticosteroids, contrast agents, neurolytic agents, and viscosupplementation are used commonly in pain management procedures. At times, medications to treat adverse reactions are required. As emphasized throughout this text, every interventional physician must be knowledgeable of the pharmacology, pharmacokinetics, and potential adverse reactions of the drugs he or she administers. Furthermore, the physician needs to be familiar with medications used to treat potential procedure complications. This chapter examines medications commonly employed during pain management procedures.

Local Anesthetics Local anesthetics are widely used and are generally safe when administered properly. Local anesthetics are therapeutically employed in most injections to provide local anesthesia or analgesia of a painful structure. The ability of local anesthetics to relieve pain can also be used diagnostically to help confirm a pain generator. Common applications include skin and soft tissue anesthesia for other procedures; intraarticular injections; injection for bursitis, tenosynovitis, entrapment neuropathies, painful ganglia; spinal injections; and nerve blocks. Local anesthetics are subdivided into esters and amides, referring to the bond that links the hydrophilic and lipophilic rings. The amide class is less allergenic and more commonly employed in local, intraarticular, and spinal injections. The most widely used agents in pain management practice are lidocaine (Xylocaine) and bupivacaine (Marcaine), both amide local anesthetics. Amide local anesthetics are hydrolyzed by the liver microsomal enzymes to inactive products. Thus, patients with hepatic failure or reduced hepatic flow are more sensitive to those agents. For this reason, patients taking beta blockers or who have congestive heart failure, have a lower maximum dosage because of their reduced hepatic flow and decreased elimination rates of the amide local anesthetics. In contrast, the ester anesthetics are rapidly hydrolyzed by plasma cholinesterase into para-aminobenzoic acid (PABA) and other metabolites that are excreted unchanged in the urine. Paraaminobenzoic acid is a known allergen in certain individuals. However, the rapid metabolism of ester local anesthetics lowers their potential for toxicity. Procaine is an amino ester commonly, but not exclusively, employed in differential spinal blocks. 2-­Cholorprocaine can be used for infiltration, epidural or peripheral nerve block, and is also an ester.

Mechanism of Action Local anesthetics exert their effect by reversibly inhibiting neural impulse transmission. The local anesthetic molecules diffuse across neural membranes to block sodium channels and inhibit the influx of sodium ions; therefore, proximity of the local anesthetic to the nerve to be blocked is required. Only a short segment of the nerve (5 to 10 mm) needs to be affected to cease neural firing. Epidural analgesia from local anesthetic is believed by some to occur because of uptake across the dura, a back door approach to spinal block. The ability of a local anesthetic to diffuse through tissues and then block sodium channels relies on the ability of these molecules to dissociate at physiologic pH of 7.4. The pKas for local anesthetics are greater than the pH found in tissue. As a result, local anesthetics in vivo exist primarily as cations, the form of the molecule that blocks the sodium channel. The base form of the local anesthetic allows it to penetrate the hydrophobic tissues and arrive at the axoplasm. In addition to host factors, neural blockade by local anesthetics is affected by the volume and concentration of local anesthetic injected, the absence or presence of vasoconstrictor additives, the site of injection, the addition of bicarbonate, and temperature of the local anesthetic.1 Increasing the total milligrams of a local anesthetic dose shortens the onset and increases the duration of the local anesthetic. Epinephrine, norepinephrine, and phenylephrine are sometimes added to local anesthetics to reverse the intrinsic vasodilation effects of many of the local anesthetics and thereby reduce their systemic absorption. This increases the amount of local anesthetic available to block the nerve. More anesthetic means a quicker onset and longer duration. Application of the local anesthetic close to the nerve improves its ability to diffuse across the axon and block sodium channels. Highly vascular sites such as the intercostal nerve and caudal epidural space tend to result in slightly shorter duration of action. The addition of bicarbonate or CO2 (700 mm Hg) to local anesthetics hasten their onset. Bicarbonate raises the pH and the amount of uncharged local anesthetic for diffusion through the nerve membrane. CO2 will diffuse across the axonal membrane and lower the intracellular pH making more of the charged form of the local anesthetic available intracellularly to block the sodium channels. Temperature elevations decrease the pKa of the local anesthetic and hasten the onset of action.

Individual Agents Local anesthetics are administered in the intradermal, subcutaneous, intraarticular, intramuscular, perineural, and epidural spaces during pain management procedures. Injections into vascular 5

6  Basic Principles of Procedures

regions such as the oral mucosa and epidural space may result in rapid absorption and higher systemic concentrations. Local anesthetics administered into or near the epidural space should be preservative free. Methylparaben is a common preservative in multidose vials and is also a common allergen.2 Lidocaine Lidocaine is the most versatile and widely used of the local anesthetics. It has a short onset of action, 0.5 to 15 minutes, and short duration of action, typically 0.5 to 3 hours. The difference between the effective dose and the toxic does is wide, resulting in a high therapeutic index compared to other common local anesthetics. Maximum doses are variably reported in the range of 400 to 500 mg of lidocaine. Typical concentrations are 0.5% to 2%. Final concentration is often diluted by the addition of a corticosteroid.1 Concentration percentages are easily converted to milligrams. For example, a 1% solution of lidocaine has 1 g of lidocaine in 100 mL of fluid. This is equivalent to 1000 mg/100 mL or 10 mg/mL. Volume of lidocaine injected varies widely with location and practitioner. Using the aforementioned guidelines, total injection of 1% lidocaine should remain below 40 mL (40 mL × 10 mg/mL = 400 mg).

Bupivicaine Bupivacaine (Marcaine) is another widely used local anesthetic. Bupivacaine’s duration of action (2 to 5 hr) is longer than lidocaine’s as is its onset of action (5 to 20 min). Bupivacaine is commonly used in concentrations of 0.125% to 0.75%. Final concentrations are often diluted by 30% to 50% by the addition of a corticosteroid. The higher concentrations generally have a faster onset of action. Bupivacaine has more cardiotoxicity than lidocaine, especially if an injection is given intravenously inadvertently. The toxic dose of bupivacaine is only 80 mg (16 mL of a 0.5% solution) when given intravascularly, but may be up to 225 mg with an extravascular injection.1

Toxicity Action of local anesthetics is affected by numerous factors reviewed above. Location of injection plays a primary role in determining the onset, duration, and toxic dose of these agents (Table 2-1). Vasoconstrictors such as epinephrine reduce local bleeding and thereby prolong the onset and duration, but are generally not employed in a pain management practice.

Table 2-1  Classification and Uses of Local Anesthetics Clinical Uses

Usual ­Concentration (%)

Usual Onset

Usual Duration (hours)

Maximum* Single Dose (mg)

Unique Characteristics

2-Chloroprocaine

Infiltration PNB Epidural

1 2 2-3

Fast Fast Fast

0.5-1.0 0.5-1.0 0.5-1.5

1000 + EPI 1000 + EPI 1000 + EPI

Lowest systemic toxicity Intrathecal route may be neurotoxic

Procaine

Infiltration PNB Spinal

1 1-2 10

Fast Slow Moderate

0.5-1.0 0.5-1.0 0.5-1.0

1000 1000 200

Used for differential spinal

Tetracaine

Topical Spinal

2 0.5

Slow Fast

0.5-1.0 2-4

80 20

Topical Infiltration IV regional PNB Epidural Spinal

4 0.5-1.0 0.25-0.5 1.0-1.5 1-2 5

Fast Fast

0.5-1.0 1-2 1-3

Fast Fast Fast

0.5-1.5

500 + EPI 500 + EPI 500 500 + EPI 500 + EPI 100

Prilocaine

IV regional PNB Epidural

4 1.5-2.0 1-3

Fast

1.5-3.0

600 600 600

Least toxic amide Methemoglobinemia possible when >600 mg

Mepivacaine

PNB Epidural

1.0-1.5 1-2

Fast Fast

2-3 1.0-2.5

500 + EPI 500 + EPI

Duration of plain solutions longer than lidocaine with EPI, useful when EPI contraindicated

Bupivacaine

PNB Epidural Spinal

0.25-0.5 0.25-0.75 0.5-0.75

Slow Moderate Fast

4-12 2-4 2-4

200 + EPI 200 + EPI 20

Exaggerated cardiotoxicity with accidental IV injection Low doses produce sensory > motor blockade

Etidocaine

PNB Epidural

0.5-1.0 1.0-1.5

Fast Fast

3-12 2-4

300 + EPI 300 + EPI

Motor > sensory blockade

Aminoesters

Aminoamides Lidocaine

EPI, epinephrine; IV, intravenous; PNB, peripheral nerve block. *Maximum single dosage is affected by many factors, this is only a guide. Modified from Barash PG, Cullen BF, Stoelting RK: Handbook of Clinical Anesthesia, 2nd ed. Philadelphia, J.B. Lippincott, 1993, pp 206-207.

Commonly Used Medications in Procedures  7

Excess amounts of local anesthetics may cause CNS effects including confusion, convulsions, respiratory arrest, seizures, and even death. The risk for complications increases if the local anesthetics are given intravascularly. Other potential adverse reactions to local anesthetics include cardiodepression, anaphylaxis, and malignant hyperthermia. Patients with decreased renal function, hepatic function or plasma esterases eliminate local anesthetics more slowly and, therefore, have an increased risk of toxicity. Toxic blood levels of lidocaine are approximately 5 to 10 μg/mL, but adverse effects can be seen at lower blood levels. Patients should be monitored for signs of toxicity including restlessness, anxiety, incoherent speech, lightheadedness, numbness, and tingling of the mouth and lips, blurred vision, tremors, twitching, depression or drowsiness. Injections into the head and neck area require the utmost care.3 Even small doses of local anesthetic may produce adverse reactions similar to systemic toxicity seen with unintentional intravascular injections of larger doses. Deaths have been reported.4 Resuscitative equipment and drugs should be immediately available when local anesthetics are used. Management of local anesthetic overdose begins with prevention by monitoring total dose administered, frequently aspirating for vascular uptake, and use of contrast to avoid vascular uptake when appropriate. Recognition of symptoms of toxicity and support of oxygenation with supplemental oxygen are keys to the initial management. Airway must be maintained and respiratory support should be provided as needed. Hypotension is the most common circulatory effect and should be treated with intravenous fluids and a vasopressor such as ephedrine in appropriate candidates. Convulsions persisting despite respiratory support are often treated with a benzodiazepine such as diazepam. If cardiac arrest occurs, standard cardiopulmonary resuscitative measures should be instituted.

Corticosteroids Corticosteroids are administered in a pain practice for their potent antiinflammatory properties. These injections to relieve pain and inflammation work well temporarily, but questions remain regarding their role in the management of many chronic musculoskeletal conditions. Corticosteroids may result in significant side effects.

The potential for these adverse effects, ranging from a relatively innocuous facial flushing effect to joint destroying avascular necrosis, must be weighed against potential benefits. Some locally injected corticosteroids are absorbed systemically and can produce transient systemic effects. Corticosteroids can be helpful in a variety of conditions including rheumatoid arthritis, bursitis, tenosynovitis, entrapment neuropathies, crystal-induced arthropathies in patients who cannot tolerate systemic treatment well, radiculopathies, and at times, osteoarthritis (OA). Corticosteroids should never be injected directly into a tendon or nerve, subcutaneous fat, or an infected joint, bursa, or tendon (Table 2-2).

Mechanism of Action All corticosteroids have both glucocorticoid, antiinflammatory, and mineralocorticoid activity. Agents with significant glucocorticoid and minimal mineralocorticoid activity include betamethasone (Celestone), dexamethasone (Decadron), methylprednisolone acetate (Depo-Medrol) and triamcinolone hexacetonide (Aristospan). Corticosteroids can be mixed in the same syringe with local anesthetics. Corticosteroids produce both antiinflammatory and immunosuppressive effects in humans. The primary mechanism of action may be their ability to inhibit the release of cytokines by immune cells.5 The effects of corticosteroids are species specific.6 Lymphocytes in humans are much less sensitive to the effects of corticosteroids than lymphocytes in common laboratory animals including the mouse, rat, and rabbit. In humans, corticosteroids reduce the accumulation of lymphocytes at inflammatory sites by a migratory effect.7 In contrast to this lymphopenia, is the neutrophilia seen by demargination of neutrocytes from the endothelium and an accelerated rate of release from the bone marrow.8 A temporary rise in white blood cell count is commonly observed for this reason after a corticosteroid dose and in isolation does not mark a post injection infection. The antiinflammatory effects of corticosteroid also occur at the microvascular level. They block the passage of immune complexes across the basement membrane, suppress superoxide radicals, and reduce capillary permeability and blood flow.9 Corticosteroids inhibit prostaglandin synthesis,10 decrease collagenase formation, and inhibit granulation tissue formation.

Table 2-2  Comparison of Commonly Used Glucocorticoid Steroids* Agent

Antiinflammatory Potency*

Salt Retention Property

Plasma Half-life (min)

Duration†

Equivalent Oral Dose (mg)

Hydrocortisone (cortisol)

1

2+

90

S

20

Cortisone

0.8

2+

30

S

25

Prednisone

4-5

1+

60

I

5

Prednisolone

4-5

1+

200

I

5

Methylprednisolone (Medrol, Depo-Medrol)

5

0

180

I

4

Triamcinolone (Aristocort, Kenalog)

5

0

300

I

4

Betamethasone (Celestone)

25-35

0

100-300

L

0.6

Dexamethasone (Decadron)

25-30

30

100-300

L

0.75

*Relative

to hydrocortisone. short; I,= intermediate; L, long. From Lennard TA: Fundamentals of Procedural Care. In Lennard TA (ed): Physiatric Procedures in Clinical Practice. Philadelphia, Saunders, 1995. †S,

2

8  Basic Principles of Procedures

The immunosuppressant effects of corticosteroids are generally via effects on T cells. These effects are not the desired effect of corticosteroid used in pain management procedures and are not observed following epidural injections.11 A review of these immunosuppressant effects can be found in other texts.11-14

Individual Agents Commonly used corticosteroid preparations include betamethasone, methylprednisolone, triamcinolone, dexamethasone, prednisolone, and hydrocortisone. Of these, betamethasone and dexamethasone have the strongest glucocorticoid or antiinflammatory effects. Corticosteroid effects can be highly variable between individuals and it is not possible to definitively state a safe dosage of corticosteroid. The following should serve only as a guide and must be tailored to each individual. Betamethasone An equal mixture of two betamethasone salts, Celestone Soluspan, allows for both immediate and delayed corticosteroid responses. Betamethasone sodium phosphate acts within hours, whereas betamethasone acetate is a suspension that is slowly absorbed over approximately 2 weeks. Betamethasone (Celestone Soluspan) is approved for intraarticular or soft tissue injection to provide short-term adjuvant therapy in osteoarthritis, tenosynovitis, gouty arthritis, bursitis, epicondylitis, and rheumatoid arthritis.15 It is also commonly employed in epidural injections. Typical intraarticular doses vary with the size of the joint and range from 0.25 to 2 mL (1.5 mg to 12 mg). Typically epidural injections range from 1 to 3 mL (6 to 18 mg). Betamethasone should not be mixed with local anesthetics that contain preservatives such as methylparaben as these may cause flocculation of the steroid. Dexamethasone Dexamethasone acetate (Decadron-LA) has a rapid onset and long duration of action. It is usually given in doses of 8 to 16 mg intramuscularly or 4 to 16 mg for intraarticular or soft tissue injections. The most common preparations have 8 mg of dexamethasone acetate per milliliter, therefore 0.5 to 2 mL quantities are the most common. Most preparations contain sodium bisulfite that can trigger allergic reactions in susceptible individuals. It contains long-acting particulates and it is not used for intravenous administration. Dexamethasone sodium phosphate (Decadron Phosphate) is a rapid onset, short duration formulation of dexamethasone. It is available in a variety of strengths ranging from 4 mg/mL to 24 mg/mL. Large joints are often injected with 2 to 4 mg, small joints 0.8 to 1 mg, bursae 2 to 3mg, tendon sheaths 0.4 to 1mg, soft tissue infiltration 2 to 6 mg.15 Sulfites are common in the preparations of this salt also. Dexamethasone is approved for the treatment of osteoarthritis, bursitis, tendonitis, rheumatoid arthritis flares, epicondylitis, tenosynovitis, and gouty arthritis.15 Because it is considered to be a nonparticulate steroid it is also used off-label for epidural steroid injections as discussed subsequently. Methylprednisolone Methylprednisolone acetate (Depo-Medrol) has 1/5 to 1/6 the glucocorticoid potency of betamethasone but similar antiinflammatory effects to prednisolone. It has an intermediate duration of action. It, like the other corticosteroids, is approved for intraarticular and soft tissue injections for short-term adjuvant therapy of osteoarthritis, bursitis, tenosynovitis, gouty arthritis, epicondylitis, and

rheumatoid arthritis.15 Depo-Medrol has been used for epidural administration also. Preparations of methylprednisolone acetate include polyethylene glycol as a suspending agent. Concerns developed as to whether the polyethylene glycol can cause arachnoiditis with (inadvertent) intrathecal injections.16 Animal studies have not demonstrated any adverse effects on neural tissues from the application of glucocorticoid.17 Methylprednisolone is now available without polyethylene glycol, PEG free. Typical doses range from 4 to 80 mg. Small joints are typically injected with 4 to 10 mg, medium joints 10 to 40mg, large joints 20 to 80 mg, bursae and peritendon 4 to 30 mg.15 Triamcinolone Triamcinolone is available as three different salts: triamcinolone diacetate (Aristocort Forte), triamcinolone hexacetonide (Aristospan), and triamcinolone acetonide (Kenalog). Duration of action is shortest with the diacetate and longest with the acetonide formulations. Triamcinolone has similar glucocorticoid activity to methylprednisolone with a long half-life. The approved uses are the same as for the agents listed earlier and it, too, is used in epidural injections. Unfortunately, it has a higher incidence of adverse reactions including fat atrophy and hypopigmentation.15

Spinal Injections Unique considerations are taken into account when considering corticosteroids for spinal injections. In particular, cervical transforaminal injections have lead to rare but significant neurologic complications such as spinal cord injury, stroke, and even death.18-22 The postulated cause of the majority of these complications is undetected vascular injections in the vertebral or spinal radicular arteries with particulate steroids causing embolic infarctions.22,23 Thoracic and lumbar transforaminal injections have similarly been implicated in neurologic complications with particulate steroids. Major complications are thought to arise from embolic events associated with injections into radicular arteries or the reinforcing radicular artery known as the artery of Adamkiewicz.24 This artery typically arises at thoracic levels but it can occur as low as L2 or L3 in about 1% of patients and more rarely at lower levels.25 Anatomic studies show that the size of particles in commonly used steroid preparations such as triamcinolone, methylprednisolone, and betamethasone equals or exceeds the caliber of many radicular arteries.26,27 These particulate steroids either are larger in diameter than a red blood cell or tend to aggregate and/or pack together to be larger than a red blood cell. This is not the case with dexamethasone sodium phosphate, which is a nonparticulate ster­ oid.27 Thus, dexamethasone sodium phosphate should reduce the risk of embolic infarcts following intravascular injections. Consistent with this, a study looked at vertebral artery injection of particulate and nonparticulate steroids in pigs while under general anesthesia. The animals that were injected with particulate steroids never regained consciousness. Subsequent magnetic resonance images (MRIs) revealed upper cervical cord and brain stem edema and histologic analysis showed ischemic changes. The animals injected with nonparticulate steroids did not have ischemic events and recovered without apparent adverse effects. The MRIs and subsequent histologic analysis were also normal in this group of animals.28 The risk with particulate steroids in cervical and thoracic transforaminal injections has led to the common use of dexamethasone sodium phosphate in these procedures. Thoracic and lumbar transforaminal injections may also lead to embolic events29-31 and this must be taken into consideration. The choice corticosteroids

Commonly Used Medications in Procedures  9

in lumbosacral transforaminal injections is debatable, especially if appropriate safety measures are used, such as contrast administration under live fluoroscopy and use of digital subtraction angiography. If vascular uptake is noted, the needle should be repositioned or the procedure aborted. Other spinal procedures such as interlaminar epidural injections or intraarticular injections have not been associated with embolic events with particulate steroids. Both particulate and nonparticulate steroids appear to be effective but studies suggest that particulate steroids may be slightly more efficacious than nonparticulate steroids.32,33 Further studies are needed to clarify this.

Adverse Reactions Corticosteroid use should be carefully considered and avoided if possible in patients at increased risk for adverse reactions, including patients with active ulcer disease, ulcerative colitis with impending perforation or abscess, poorly controlled hypertension, congestive heart failure, renal disease, psychiatric illness or history of steroid psychosis, or a history of severe or multiple allergies.15,34 Intraarticular injections have been associated with osteonecrosis, infection, tendon rupture, postinjection flare, hypersensitivities, and systemic reactions.15 Intraspinal injections have been associated with adhesive arachnoiditis, meningitis, and conus medullaris syndrome.16 Adverse reactions to injected corticosteroids include a transient flare of pain for 24 to 48 hours in up to 10% of patients. Diabetics and those individuals with a predisposition to diabetes may become hyperglycemic and appropriate monitoring and corrective measures should be instituted. Adrenal cortical insufficiency is generally not seen associated with intermittent injections of corticosteroids, but remains a serious adverse reaction that could be precipitated by indiscriminate, frequent high-dose corticosteroid injections. Allergic reactions to systemic glucocorticoids have been reported and if slow release formulations are used, the allergic response may not occur until a week after the injection.35 Even with local injections of corticosteroids, some systemic response may occur. Generally less serious side effects of corticosteroids include facial flushing, injection site hypopigmentation, subcutaneous fat atrophy, increased appetite, peripheral edema or fluid retention, dyspepsia, malaise, and insomnia.15 Prolonged or repeated doses can result in cushingoid changes.

Drug Interactions A number of drug-drug interactions for corticosteroids have been reported. Some of the more common ones encountered in a pain management practice are mentioned here. Estrogens and oral contraceptives may potentiate the effect of the corticosteroid. Macrolide antibiotics (e.g., erythromycin, azithromycin) may greatly increase the effect of methylprednisolone by decreasing its clearance. In contrast, the hydantoins (e.g., phenytoin), rifampin, phenobarbital, and carbamazepine may increase corticosteroid clearance and decrease the antiinflammatory therapeutic effect. Theophylline and oral anticoagulants can interact variably with corticosteroids.15

Neurolytic Agents Neurolytic drugs such as phenol are employed in pain management practice primarily to treat spasticity. Neurolytic agents also have been used for treating chronic pain including intractable cancer

pain and facet denervation procedures. The use of neurolytic agents for facet joint neurotomies is being replaced by radiofrequency lesioning.36,37 Neurolytic agents are nonspecific in destroying all nerve fiber types. Phenol, ethyl alcohol, propylene glycol, chlorocresol, glycerol, cold saline, and hypertonic and hypotonic solutions have been employed as neurolytics. Of these, phenol is the most studied and widely used neurolytic.

Phenol Phenol is the most widely instilled agent to treat severe spasticity. Phenol can be injected around a motor nerve to selectively reduce hypertonicity.38,39 Intrathecal injections of phenol have been used to treat spasticity of spinal cord origin and intractable pain disorders. Sympathectomies for peripheral vascular disease have also been accomplished by injection of phenol along the paravertebral and perivascular sympathetic fibers.40,41

Mechanism of Action Phenol (carbolic acid) denatures protein and thereby causes denervation. Histologic sections show nonselective nerve destruction, muscle atrophy, and necrosis at the site of phenol injections.42-44 Higher concentrations of phenol are associated with greater tissue destruction. Optimal concentration has not been determined and long-term difference between injection of 2% and 3% solution have not been noted.44 Denervation potentials are seen as early as 3 weeks following phenol blocks.45 Clinical response of decreased pain or spasticity last between 2 months and 2 years irrespective of underlying disorder.43,44 Endoneural fibrosis is seen following phenol injections and is believed to impede reinnervation of the muscle by slow wallerian regeneration.

Dosage Phenol is placed in an aqueous solution, glycerin or lipids for administration. Commercially available phenol is an 89% solution and must be diluted to the desired concentration, typically 2 to 3%. Commonly it is mixed with equal part glycerin and then diluted with normal saline to 2% to 5%. The maximum daily injectable dose is 1 g. Toxic effects are uncommon in doses ≤100 mg. Phenol is eliminated through the liver; use in patients with significant liver disease should be avoided.

Adverse Reactions Local reactions to phenol injection include delayed soreness from the associated necrosis and inflammation.42 This discomfort can be relieved with ice packs and analgesics and typically resolves within 24 hours. If the needle is withdrawn without flushing it with saline, phenol may come in contact with the skin and cause erythema, sloughing, and skin necrosis. Protective eyewear can minimize the chance of eye irritation—conjunctivitis from any phenol splashing into the patient’s or physician’s eyes. Paresthesias or dysesthesias from mixed somatic nerve blocks are probably due to an incomplete block. Paresthesias/dysesthesias occur in up to 25% of nerve blocks and resolve within 3 months.38,46-55 Repeat blocks often alleviate these symptoms indicating the dysesthesias may stem more from an incomplete block than from phenol-induced dysesthesias. Systemic reactions to phenol are usually the result of inadvertent intravascular or central blockade.56-59 Adverse systemic

2

10  Basic Principles of Procedures

reactions most commonly affect the cardiovascular and central nervous systems.58 Cardiac dysrhythmias, hypotension, venous thrombosis, spinal cord infarcts, cortical infarcts, meningitis, and arachnoiditis have been reported.58,60,61

Contrast Agents Contrast agents are administered to help visualize the location of the needle tip, confirm the flow of injectant or visualize the involved structure (e.g., joint, bladder, bursa). Inadvertent vascular uptake despite negative aspiration is not uncommon. The toxicity of local anesthetics and corticosteroids increases with intravascular injection and contrast-enhanced fluoroscopic guidance helps minimize these toxicities. Contrast agents are all iodinated compounds that allow opacification of structures for visualization. Contrast media is divided into ionic and nonionic agents. The nonionic contrast agents are low osmolality and may decrease the potential for adverse reactions. Although these nonionic agents decrease minor reactions such as nausea and urticaria, they have not been shown to decrease the incidence of more severe reactions.62,63 They do not eliminate the possibility of severe or fatal anaphylactic reactions. Potential for adverse reaction can be minimized by limiting the quantity of the contrast media injected and adequately screening patients. Patients with a history of contrast reaction, significant allergies, impaired cardiac function/limited cardiac reserve, bloodbrain barrier breakdown, and severe anxiety are at increased risk for generalized reactions including urticaria, nausea, vomiting, and anaphylaxis. Patients with impaired renal function and paraproteinemias are at increased risk for renal failure with the administration of contrast agents. Renal complications can be minimized by limiting the volume of contrast agent, ensuring adequate hydration before, during, and after the procedure and using the low osmolality agents for patients more than 70 years with Cr ≥ 2 mg/dL. Spinal procedures including epidural steroid injections, facet joint injections, sympathetic blocks, discography, spinal nerve blocks, and sacroiliac joint injections are all ideally performed with the aid of fluoroscopy and contrast enhancement.64,65 The nonionic contrast agents are used for these injections because the potential for subarachnoid spread exists with any of these procedures. The two most common nonionic agents are iopamidol (Isovue) and iohexol (Omnipaque). Both agents are nonionic, readily available as an injectable liquid, water soluble and quickly cleared. The first of the nonionic contrast agents, metrizamide (Amipaque), is a powder which must be reconstituted. Metrizamide also is associated with a higher incidence of seizures than either iohexol or iopamidol and is rarely used now for procedures. Generally, 0.2 to 2 mL of nonionic contrast is sufficient for the experienced injectionist to confirm location and spread of the contrast. These agents are 90% eliminated through the kidneys within 24 hours. Side effects are uncommon but include nausea, headaches, and CNS disturbances.66 Ionic contrast agents such as diatrizoate (Renografin) and iothalamate (Conray) can be used for other contrast enhanced injections including arthrograms, cystometrograms, and bursa injections. These agents are well tolerated in these situations when total volume of contrast is limited to 15mL or less.

Premedication for Allergic Reactions The risk of anaphylactoid reactions is 1% to 2% when radiopaque agents are used. This risk increases to 17% to 35% when repeat exposure to radiopaque agents occurs in individuals with known

sensitivities.54,66-68 If premedication with diphenhydramine and methylprednisolone is given, the risk of anaphylactoid reactions is reduced to approximately 3.1%.66 The current recommended prophylactic protocol is methylprednisolone 32 mg by mouth 12 and 2 hours prior to contrast use.69 Concurrent use of specific H1 and H2 blockers is also recommended.70,71

Viscosupplementation Viscosupplemenation with hyaluronic acid (HA) injections is FDA approved for knee osteoarthritis although it is sometimes used off-label for osteoarthritis of other joints.Hyaluronic acid is a large macromolecule, a glycosaminoglycan composed of repeating disaccharides of glucuronic acid and N-acetylglucosamine, that is naturally occurring in synovial fluid. It is a viscous component of synovial fluid and acts as a lubricant and cushion for joints. In osteoarthritis, the synovial fluid breaks down into smaller units, thereby decreasing its lubricating and shock-absorbing abilities. HA injections are believed to improve the elastoviscosity of the arthritic joint by increasing the HA concentration. Commonly available agents are Hyalgan (hyaluronate sodium), Orthovisc (hyaluron), Supartz (hyaluronan), Synvisc and SynviscOne (hylan GF-20). These are given once a week over 3 to 5 weeks depending on the agent used. The one exception is Synvisc-One, which is injected once. Several randomized controlled trials have demonstrated that viscosupplementation is superior to placebo but the clinical efficacy is likely modest.72 A 2003 meta-analysis in JAMA looking at 22 trials concluded that HA was superior to placebo injections but had a relatively small effect. The effect was probably similar to NSAIDs. It also raised concern about a possible publication bias with 17 of 22 trials being industry sponsored, which may overestimate effects of viscosupplementation.73 Another meta-analysis in 2004 looked at 13 randomized controlled trials and found that it is an effective treatment for patients with knee OA who have ongoing pain or are unable to tolerate conservative treatment or joint replacement. HA appears to have a slower onset than intraarticular steroid injections and may last longer.74 A more recent review of viscosupplementation suggested that clinical improvement attributable to viscosupplementation is likely small.75 Adverse reactions with HA injections are generally mild but reports vary regarding frequency. Mild side effects include pain at injection site (1% to 33%), local joint pain and swelling (<1% to 30%) and local skin reactions (3% to 21%). A pseudoseptic reaction can occur but is uncommon (1% to 3%).75 In summary, viscosupplementation is FDA approved for knee osteoarthritis. Randomized controlled studies have demonstrated that it is superior to placebo but the clinical effect appears to be small to modest. Some of these studies suggest that it is as efficacious as the use of NSAIDs. When other conservative measures fail or are not an option, viscosupplementation may be a viable alternative for knee osteoarthritis.

Treatment of Medication Adverse Reactions Medication adverse reactions can be minimized by careful patient selection and vigilance during the procedure. However, it is impossible to completely eliminate the possibility of allergic or other reactions and the practitioner must be prepared to deal with these emergency situations. Immediate access to and familiarity with emergency medications and protocols is critical.

Commonly Used Medications in Procedures  11

Minor medication reactions can be treated with observation to ensure symptoms do not worsen. Moderate reactions can be treated in the procedure area and do not require hospitalization. These reactions include symptomatic urticaria, bronchospasm, and vasovagal reactions. Symptomatic urticaria can be treated with 25 to 50 mg of diphenhydramine IM. Bronchospasm should be treated with supplemental oxygen by nasal cannula and O2 saturation monitoring, intravenous access, and electrocardiogram monitoring. If needed, a beta agonist inhaler can be administered as long as bronchospasm has not worsened to laryngotracheal edema. Epinephrine 1:1000 is sometimes required in doses of 0.1 to 1 mL subcutaneously. In refractory bronchospasm and more severe reactions of laryngotracheal edema or symptomatic facial edema, intravascular epinephrine 1:10,000 is given in doses of 1 to 3 mL. Vasovagal reactions are heralded by symptomatic bradycardia and hypotension. With early reaction these symptoms can often be aborted with simple measures of reassurance, leg elevation, and intravenous fluids. Vital signs must be monitored and supplemental oxygen should be initiated promptly if oxygen saturation begins to drop. For more severe vasovagal reactions, drops in blood pressure and pulse can be treated with atropine 0.3 to 0.5 mg IV given incrementally up to 2 mg. Vasovagal reactions with hypotension and bradycardia must be distinguished from anaphylactoid or cardiac reaction where the hypotension is associated with tachycardia. Toxic convulsions may be treated with oxygen, airway management, and diazepam 1 to 10 mg intravenously in 1 mg increments. Hospitalization is recommended along with appropriate consultation. Cardiopulmonary arrest should be treated following standard advanced cardiac life support protocols: assess vital signs, secure airway and oxygenation, begin resuscitation, ensure intravenous access, follow appropriate treatment algorithm. After successful resuscitative attempts, the patient should be hospitalized for observation and any necessary treatment.

Conclusion Pain physicians commonly use a core group of medications for their procedures. It is imperative the injectionist has a solid understanding of these agents to maximize benefit and minimize risk. Integration of injection procedures in appropriately selected patients increases the physician’s effectiveness. REFERENCES   1. Williams MJ. Pharmacology for regional anesthetic techniques. In: Hahn MB, McQuillan PM, Sheplock GJ, eds. Regional anesthesia: An atlas of anatomy and techniques. St. Louis: Mosby-Year Book; 1996:3-17.   2. SchorrParaben Allergy WF, Jama. 1968; 204:107-110.   3. Covino BG. Clinical pharmacology of local anesthetic agents. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and pain management. Philadelphia: J.B.Lippincott; 1996:111-144.   4. Olin BR. Miscellaneous products: Local anesthetics, injectable. In: Olin BR, ed. St. Louis: Wolters Kluwer; 1993:2654-2665.   5. Crabtree GR, Gillis S, Smith KA, Munck A. Glucocorticoids and immune responses.[Review]. Arthritis Rheum. 1979;22(11):1246-1256.   6. Claman HN. Corticosteroids and lymphoid cells. N Engl J Med. 1972; 287(8):388-397.   7. Peters WP, Holland JF, Senn H, et al. Corticosteroid administration and localized leukocyte mobilization in man. N Engl J Med. 1972;286(7):342-345.

  8. Fauci AS, Dale DC, Balow JE. Glucocorticosteroid Therapy: Mechanism of action and clinical considerations. Ann Intern Med. 1976; 84(3):304-315.   9. Schayer RS. Synthesis of histamine, microcircularoty regulation and the mechanisms of action of the adrenal glucocorticoid hormones. Prog Allergy. 1963;7:187. 10. Robinson DR. Prostaglandins and the mechanism of action of antiinflammatory drugs.[Review]. Am J Med. 1983;75(4B):26-31. 11. Robinson JP, Brown PB. Medications in low back pain. Phys Med Rehabil Clin North Am. 1991;2:97-126. 12. Brown PB. The use of steroidal agents in the oral route. In: Wilkens RF, Dali SL, eds. Therapeutic Controversies in the Rheumatic Diseases. Orlando: Grune and Stratton; 1987, p 71. 13. Cupps RR, Fauci AS. Corticosteroid-mediated immunoregulation in man.[Review]. Immunol Rev. 1982;65:133-155. 14. Fauci AS, Dale DC, Balow JE. Glucocorticosteroid therapy: mechanism of action and clinical considerations. Ann Intern Med. 1976; 84(3):304-315. 15. Olin BR, ed. Facts and Comparisons. St Louis: Wolters Kluwer; 1993: 458-486. 16. Nelson DA. Intraspinal therapy using methylprednisolone acetate. Spine. 1993;18:278-286. 17. Delaney T, Rowlingson RC, Carron H. Epidural steroid effects on nerve and meninges. Anesth Analg. 1980;59:610-614. 18. McMillan MR, Crumpton C. Cortical blindness and neurologic injury complicating cervical transforaminal injection for cervical radiculopathy. Anesthesiology. 2003;99:509-511. 19. Rozin L, Rozin R, Koehler SA, et al. Death during a transforaminal epidural steroid nerve root block(C7) due to perforation of the left vertebral artery. Am J Forensic Med Path. 2003;24:351-355. 20. Tiso RL, Cutler T, Catania JA, Whalen K. Adverse central nervous system sequelae after selective transforaminal block: The role of corticosteroids. Spine J. 2004;4:468-474. 21. Brouwers PJAM, Kottnik EJBL, Simon MAM, Prevo RL. A cervical anterior spinal artery syndrome after diagnostic blockade of the right C6-nerve root. Pain. 2001;91:397-399. 22. Baker R, Dreyfuss P, Mercer S, Bogduk N. Cervical transforaminal injection of corticosteroids into a radicular artery: A possible mechanism for spinal cord injury. Pain. 2003;103:211-215. 23. Rathmell JR, Aprill C, Bogduk N. Cervical transforaminal injection of steroids. Anesthesiology. 2004;100:1595-1600. 24. Bogduk N, Dreyfuss P, Baker R, et al. Complications of spinal diagnostic and treatment procedures. Pain Med. 2008;9:S11-S34. 25. Lo D, Vallee JN, Spell L, et al. Unusual origin of the artery of Adamkiewicz from the fourth lumbar artery. Neuroradiology. 2002;44:153–17. 26. Tiso RL, Cutler T, Catania JA, Whalen K. Adverse central nervous system sequelae after selective transforaminal block: The role of corticosteroids. Spine J. 2004;4:468-474. 27. Derby R, Date E, Lee CH, et al. Size and aggregation of corticosteroids used for epidural injections. Interventional Spine. ISIS Newsletter. 2005;5(4):30-37. 28. Okubadejo GO, Talcott MR, Schmidt RE, et al. Perils of intravascular methylprednisolone injection into the vertebral artery. An animal study. J Bone Joint Surg Am. 2008;90:1932-1938. 29. Somyaji HS, Saifuddin A, Casey ATH, Briggs TWR. Spinal cord infarction following therapeutic CT-guided left L2 nerve root injection. Spine. 2005;30:E106-E108. 30. Houten JK, Errico TJ. Paraplegia after lumbosacral nerve root block: Report of three cases. Spine J. 2002;2:70-75. 31. Quintero N, Laffont I, Bouhmidi L, et al. Transforaminal epidural steroid injection and paraplegia: Case report and bibliographic review. Ann Readapt Med Phys. 2006;49:242-247. 32. Dreyfuss P, Baker R, Bogduk N. Comparative effectiveness of cervical transforaminal injections with particulate and nonparticulate corticosteroid preparations for cervical radicular pain. Pain Med. 2006;7:237-242. 33. O’Donnell C, Cano W, Eramo G. Comparison of triamcinolone to dexamethasone in the treatment of low back pain and leg pain via lumbar transforaminal epidural steroid injection. Spine J. 2008;8:S65.

2

12  Basic Principles of Procedures 34. Goebert HW, Jallo SJ, Gardner WJ, Wasmuth CE. Painful radiculopathy treated with epidural injections of procaine and hydrocortisone acetate: Results in 113 patients. Anesth Analg. 1961;140:130-134. 35. Preuss L. Allergic reactions to systemic glucocorticoids: A review. Ann Allergy. 1985;55:772-775. 36. Dreyfuss P, Halbrook B, Pauza K, et al. Lumbar percutaneous RF medial branch neurotomy for chronic zygapophysial joint pain—a pilot study. Denver: International Spinal Injection Society; 1997. 37. Lord SM, Barnsley L, Wallis BJ, et al. Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. New Engl J Med. 1996;335(23):1721-1726. 38. Khalili AA, Harmel MH, Forster S, et al. Management of spasticity by selective peripheral nerve block with dilute phenol solutions in clinical rehabilitation. Arch Phys Med Rehabil. 1964;45:513-519. 39. Wood KM. The use of phenol as a neurolytic agent: A review. Pain. 1978;5:205-229. 40. Hughes-Davies DI, Redman LR. Chemical lumbar sympathectomy. Anesthesia. 1976;31:1068-1075. 41. Reid W, Watt JK, Gray TG. Phenol injections of the sympathetic chain. Br J Surg. 1970;57:45-50. 42. Garland DE, Lucie RS, Waters RI. Current uses of open phenol nerve block for adult acquired spasticity. Clin Orthop Rel Res. 1982; 165:217-222. 43. Halpern D. Histologic studies in animals after intramuscular neurolysis with phenol. Arch Phys Med Rehabil. 1977;58:438-443. 44. Mooney V, Frykman G, McLamb J. Current status of intraneural phenol injections. Clin Orthop Relat Res. 1969;63:122-131. 45. Brattstrom M, Moritz U, Svantesson G. Electromyographic studies of peripheral nerve block with phenol. Scand J Rehabil Med. 1970;2:17-22. 46. Copp EP, Harris R, Keenan J. Peripheral nerve block and motor point block with phenol in the management of spasticity. Proc R Soc Med. 1970;63:937-938. 47. Copp EP, Keenan J. Phenol nerve and motor point block in spasticity. Rheum Phys Med. 1972;11:287-292. 48. Katz JK, Knott LW, Feldman DJ. Peripheral nerve injections with ­phenol in the management of spastic patients. Arch Phys Med Rehabil. 1967;48:97-99. 49. Khalili AA. Physiatric management of spasticity by phenol nerve and motor point block. In: Ruskin AP, ed. Current Therapy in Physiatry. Philadelphia: Saunders; 1984, 464-474. 50. Khalili AA, Betts HB. Peripheral nerve block with phenol in the management of spasticity. Indications and complications. JAMA. 1967;200:1155-1157. 51. Petrillo C, Chu D, Davis S. Phenol block of the tibial nerve in the hemiplegic patient. Orthopedics. 1980;3:871-874. 52. Petrillo C, Knoploch S. Phenol block of the tibial nerve for spasticity: A long-term follow-up study. Int Disabil Stud. 1988;10:97-100. 53. Reeves KD, Baker A. A mixed somatic peripheral phenol nerve block for painful or intractable spasticity: A review of 30 years of use. Am J Pain Manage. 1992;2:205-210. 54. Shehadi WH. Contrast media adverse reactions: Occurrence, recurrence and distribution patterns. Radiology. 1982;143(1):11-17. 55. Spira R. Management of spasticity in cerebral palsied children by peripheral nerve block with phenol. Dev Med Child Neurol. 1971;13: 164-173.

56. Benzon HT. Convulsions secondary to intravascular pheno: A hazard of celiac plexus block. Anesth Analg. 1979;58:150-151. 57. Holland AJC, Yousseff M. A complicaton of subarachnoid phenol blockade. Anesthesia. 1979;34:260-262. 58. Swerdlow M. Complications of neurolytic neural blockade. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain. New York: J.B. Lippincott; 1988:719-735. 59. Totoki T, Kato T, Nomoto Y, et al. Anterior spinal artery syndrome: A complication of cervical intrathecal phenol injections. Pain. 1979; 6:99-104. 60. Macek C. Venous thrombosis results from some phenol injections. JAMA. 1983;249:1807. 61. Morrison JE Jr, Matthews D, Washington R, et al. Phenol motor point blocks in children: Plasma concentrations and cardiac dysrhythmias. Anesthesiology. 1991;75:359-362. 62. Lawrence V, Matthai W, Hartmaier S. Comparative safety of highosmolality and low-osmolality radiographic contrast agents. Report of a multidisciplinary working group. Invest Radiol. 1992;27:2-28. 63. Steinberg EP, Moore RD, Powe NR, et al. Safety and cost effectiveness of high-osmolality as compared with low-osmolality contrast material in patients undergoing cardiac angiography. N Engl J Med. 1992;326(7):425-430. 64. Renfrew DL. Correct placement of epidural steroid injections: Fluoroscopic guidance and contrast administration. Am J Neuroradiol. 1991;12:1003-1007. 65. White AH, Derby R, Wynne G. Epidural injections for diagnosis and treatment of low-back pain. Spine. 1980;5:78-86. 66. Olin BR. Miscellaneous products: Radiopaque agents. In: Olin BR, ed. Facts and Comparisions. St. Louis: Wolters Kluwer.; 1993:2824-2831. 67. Caro JJ, Trindade E, McGregor M. The risks of death and of severe nonfatal reactions with high- vs. low-osmolality contrast media: A metaanalysis. Am J Roentgenol. 1991;156:825-832. 68. Katayama H, Yamaguchi K, Kozuka T, et al. Adverse reactions to ionic and nonionic contrast media: A report from the Japanese Committee on the Safety of Contrast Media. Radiology. 1990;175:621-628. 69. Lasser EC, Berry CC, Talner LB, et al. Pretreatment with corticosteroids to alleviate reactions to intravenous contrast material. N Engl J Med. 1987;317(14):845-849. 70. Cusmano J. Premedication regimen eases contrast reaction. Diagn Imaging. 1992:181-182, 185-186. 71. Greenberger PA, Patterson R. The prevention of immediate generalized reactions to radiocontrast media in high-risk patients. J Allergy Clin Immunol. 1991;87:867-872. 72. Roberts WN, Furst DE, Romain PL. Intraarticular and soft tissue injections: What agent(s) to inject and how frequently? Uptodate.com. 2009;17:1. 73. Lo GH, LaValley M, McAlindon T, Felson DT. Intra-articular hyaluronic acid in treatment of knee osteoarthritis: A meta-analysis. JAMA. 2003;290:3115. 74. Aggarwal A, Sempowski IP. Hyaluronic acid injections for knee osteoarthritis. Systematic review of the literature. Can Fam Physician. 2004;50:249-256. 75. Woods S, Davis E, Schechtel M, et al. Three treatments for osteoarthritis of the knee: Evidence shows lack of benefit. Agency for Healthcare Research and Quality. U.S. Department of Health and Human Services. 2009.

Psychological Aspects of Pain

3

Dale A. Halfaker, PhD, Steven T. Akeson, PsyD, Danielle R. Hathcock, MS, Curtis Mattson, MS, and Ted L. Wunderlich, BA

The evolution of the definition of pain and the influence of the importance of various biopsychosocial factors can be observed through various theories, all of which attempt to provide a better understanding of the process of pain. One universal assumption held by each of these theories is of pain as a subjective experience, meaning that each individual may subjectively feel, experience, and interpret the meaning of their pain uniquely.

Models of Pain Gate-Control Theory of Pain The first major modernized medical model theory of pain, the gate-control theory, emphasized the close interaction between psychosocial and physiologic processes. The gate-control theory of pain describes how thoughts, feelings, and behavior affect pain.1,5 The hypothesis is that a “gate,” located within the human brain, determines the individual’s impression of pain. The gate may be opened or closed—this determines the amount of pain the individual experiences. The underlying assumption is that the pain message originates at the site of aggravation, the signal is transmitted to the brain, and the pain is then brought into the individual’s awareness. There are many ways in which an individual may “open” or “close” the gate. Using coping strategies may close the gate (meaning that the brain will either not recognize or give credence to the pain signal), while allowing oneself to focus on thoughts of pain may open the gate (bringing the pain signal into the brain’s awareness). Negative thinking, nonconstructive, pessimistic thinking may also open the gate, as will stress, anxiety, tension, helplessness, anger, hopelessness, and despair. The ultimate conclusion from this theory is that the process of pain can therefore be mediated by changing the way an individual cognitively processes the pain experience. This theory is often useful in clinical practice as a means of explaining pain to patients, and aids the clinician in treating pain via cognitive therapy; however, the scientific community has demanded a more comprehensive theory that accounts for the neurophysiology, neurotransmission, and opioid receptors that may all be involved in understanding and defining pain. This demand was the precursor to the neuromatrix model of pain.

Neuromatrix Model of Pain The term neuromatrix refers to the neural network involved in the perception of pain. The neuromatrix theory integrates physiologic and psychological evidences, and assumes pain to be a multifaceted experience, with pain sensations produced by specific patterns of nerve impulses generated by a widely distributed neural network. The neuromatrix model may be viewed as a diathesis-stress approach, meaning that predispositional factors interact with acute stressors to result in a pathologic state. The experience of pain might be thought of as such a stressor. Further explained, the theory proposes that when an organism is injured, there is an interruption of homeostatic regulation. This disruption is not only physically stressful, but it also creates psychological stress. This in turn initiates a complex response aimed at restoring homeostasis (homeostasis being the previously nonpainful state of the body). This process of homeostatic restoration can add further physical and psychological stress. Physiologically, the body may experience deleterious effects, such as immune system suppression, hypertension, and physical discomfort such as stomach pains or heart burn. The psychological aspects of pain result in the body activating the limbic system. The limbic system plays an important role in experiencing and regulating emotions, motivation of actions, and contributes to thought patterns. In the case of pain, one’s subjective interpretation of the pain experience, fear, and anxiety all further remove the body from homeostasis. Thus, once pain is established and the body activates the necessary mechanisms to return to homeostasis, any future or additional experience of pain will be physiologically and psychologically viewed as a continual threat that creates harmful demands on the body. Thus, a cycle develops that contributes to and maintains the pain-stress process. The neuromatrix hypothesis suggests that an individual’s unique genetic makeup and his or her own subjective experience of pain are the chief components that determine the nature of the pain the organism will experience and is the basis for individual differences in the pain experience. Both the gate-control theory and the neuromatrix model have attempted to integrate and define a great deal of psychological and physiologic scientific data, although it is thought neither of them provides a fully adequate theory to define the pain experience. They do, however, point to what is currently the most promising approach to understanding pain: the biopsychosocial approach. This approach views physical disorders, including pain, as the result of 13

14  Basic Principles of Procedures

a dynamic interaction between physiologic, psychologic, and social factors that can heavily influence a subject’s clinical presentation.

Biopsychosocial Model of Pain In an effort to explain why individual experiences of pain are unique, the biopsychosocial model examines how psychological, social, and economic factors can interact with physical pathology to modulate a patient’s report of symptoms and subsequent disability. This understanding has been the foundation for a major paradigm shift in the assessment and management of pain, moving away from a traditional biomedical reductionist approach to this more comprehensive biopsychosocial approach. In fact, this paradigm shift is so dramatic that it has resulted is a mandate from the Joint Commission on the Accreditation of Healthcare Organizations requiring physicians to consider pain as a fifth vital sign. The Pain Care Bill of Rights of the nonprofit American Pain Foundation calls for management of all types of pain, both malignant and nonmalignant. In order to understand pain in view of the biopsychosocial model, it seems helpful to examine the distinction between disease and illness. The term disease is generally used to define “an objective biological event” that involves the disruption of specific body structures or organ systems, caused by anatomic, pathologic, or physiologic changes. Illness, in contrast, is generally defined as a subjective experience or self-attribution of disease being present. An illness will yield physical discomfort, behavioral limitations, and psychosocial distress. Therefore, illness references how a sick individual and members of his or her family live with and respond to symptoms and their resulting disabilities. To illustrate this distinction between disease and illness is analogous to the distinction made between nociception and pain. Nociception involves the stimulation of nerves that convey information about tissue damage to the brain. Pain, however, is a more subjective perception that is the result of the transduction, transmission, and modulation of sensory input, and may be filtered through an individual’s genetic composition, prior learning history, current physiologic status, and sociocultural influences. The combination of the physiologic experience of pain and the debilitating behavior that can accompany it are the expressions of suffering and pain behavior. Based on this notion, it is thought that pain cannot be comprehensively assessed without a full understanding of the person who is exposed to the nociception. The biopsychosocial model focuses on illness. With this perspective, diversity in pain behavior can be expected as illness experience varies from person to person. This may include severity, duration, and psychological consequences. The interrelationships among biologic changes, psychological status, and the social and cultural context all need to be taken into account in fully understanding the pain patient’s perception of and response to illness. A model or treatment approach that focuses on only one of these core set of factors will be insufficient to effectively assess and treat the patient. The biopsychosocial model has consistently demonstrated the heuristic technique in treatment.2 When interpreting pain using the biopsychosocial model, clinicians should be aware that each of the three constructs in the model are different in their composition. Therefore, their assessment will be accomplished through different means and processes. Pain likely should be viewed longitudinally as an ongoing, multifactorial process in which there is dynamic interplay between the biologic, psychological, and social cultural factors that shape the experience and responses of patients.2,5

To comprehensively assess pain, it is important to account for potential interactions in the process of prescribing the best treatment regimen, individualized for a particular patient with pain. For example, a patient may present with pain resulting from an earlier accident that produced severe musculoskeletal injuries, such as bone fractures and ligament tears, that have not completely healed. In addition to these physical injuries and resultant pain, the accident may have led to the inability to return to work. The patient might also have self-esteem problems because he or she is viewed as being disabled and is stigmatized by this situation. This may have resulted in economic problems and stressors because of the sudden decrease in income. There are debts to be paid, causing family stress, turmoil, and guilt. If this patient comes from a culture in which work and activity are highly valued there may be even more psychosocial distress. Thus, there are potentially multiple levels of psychosocial stressors that all need to be assessed and considered before one can develop a comprehensive pain management program for a patient who may not be responding to conventional or conservative care as might be expected. Another model outlined four dimensions associated with the concept of pain: (1) nociception (2) pain (3) suffering and (4) pain behavior.3,5 Nociception refers to the actual physical units that might affect specialized nerve fibers and signal the central nervous system that an aversive event has occurred. This may include chemical irritant, physical/mechanical, or thermal pain. Pain is the sensation arising as the result of perceived nociception. However, this definition is overly simplistic because sometimes pain is perceived in the absence of nociception. An example of this would be phantom limb pain. On the contrary nociception has been recorded to occur without being perceived, such as an individual who is in shock after experiencing a very severe injury. Nociception and pain act as signals to the central nervous system. Suffering is a reaction to these signals that can be affected by past experiences as well as anticipation of future events, and refers to the emotional association with it, such as fear, threat, or loss.3 Because of a specific painful episode, anxiety and depression may develop as a consequence to the pain behavior. Pain behavior refers to things that individuals do when they are suffering or currently experiencing pain. For example, a person may avoid driving after experiencing an injury due to an accident. The implications for pain behavior can range from avoiding certain activities to more debilitating problems such as developing generalized anxiety surrounding any activity the person must participate in to have a functional life. As such, the interaction in the range of biopsychosocial factors can be quite broad. There are times when the nature of the patient’s response to treatment may have less to do with the objective physical condition than it does with their psychological receptivity to treatment as well as their expectations. This is the grist for the mill of the psychological evaluation and psychotherapy-related treatment process of the person with pain.

Psychological Evaluation Because of the biopsychosocial complexity associated with pain, pain-related psychological evaluation can be helpful in cases in which symptoms are in excess of expectation or do not correlate with known physiologic processes. Psychological factors may be producing delayed recovery of function or preventing the individual from otherwise benefiting from appropriate medical treatment which, if identified, can improve the treatment process and the ultimate outcome of the case.

Psychological Aspects of Pain  15

If psychological factors are identified as moderating or mediating the patient’s pain-related behavior, it can result in treatment recommendations that remove or ameliorate the barriers to improvement and recovery. Thus, it is thought to be helpful for treating physicians to have a basic understanding of the painrelated psychological evaluation and treatment process. The psychological evaluation of patients with pain begins with the establishment of rapport with the individual to be assessed. In a psychology practice it is not unusual to initially encounter a patient with pain who enters the evaluation room defensively at best and offended, angry, and/or suspicious at worst. The patient with pain may interpret the pain-related psychological consultation to imply the referral source believes their problems are not real or that their complaints are psychogenic in origin. For this reason, in addition to addressing issues of informed consent and establishing rapport with the patient, there is usually a need to provide some education as to the purpose of the evaluation and how biopsychosocial variables fit into the clinical picture and subjective situation of the patient’s life. It can be extremely helpful for the referring physician to approach the referral for a pain-related psychological evaluation in a sensitive, compassionate manner. We suggest initially explaining to patients that the dualistic view in which the mind and body are separate does not appear to hold true, and that there is a dynamic, interdependent relationship between the individual’s psyche and their physical condition. We have found it makes sense to our patients when we explain our goal to be to treat the whole person and that we want to ensure they are as psychologically and mentally fit as they can be while they are in the process of physically rehabilitating and becoming more physically fit following an injury or in treating their painful condition. The basic purpose of the pain-related psychological evaluation is to answer the questions posed by the referral source as clearly as possible. Often, if no referral questions are forwarded with the referral, the consulting psychological examiner may need to call the referral source to clarify if there are any specific issues that need to be addressed in the evaluation. Another goal of the evaluation is to generate psychological and behavioral information that is helpful to the referral source in understanding the psychological issues in the case and promotes the care in a more efficient and effective manner. The psychological evaluation documents and preserves a record of the assessment for use in the future and may provide a baseline or outcome information regarding progress. Ultimately, appropriate diagnosis leading to specific, practical, and functional recommendations that advance the patient’s care in a meaningful way become the goal for appropriate evaluation.4 To achieve the purposes of the evaluation, sufficient records need to be gathered and reviewed to provide an understanding of the medical issues and physiologic underpinnings of the case. A comprehensive clinical interview is necessary to elicit historical information about the onset and history of the pain, injuries, and background that may be psychologically contributing to the onset, severity, exacerbation, or maintenance of the pain. Opportunities for behavioral observation when the patient may or may not be aware he or she is being observed provide excellent data regarding the consistency of subjective complaints. Psychological testing can provide data derived from standardized samples of behavior that are quantifiable and illustrate how the individual being evaluated deviates from a normative base related to the concepts that are being assessed. The clinical interview in these cases tends to be comprehensive in nature and covers important factors that can serve as potential barriers to recovery. Important topics for the clinical interview should likely include an understanding of the person’s cultural and ethnic background, because various cultures deal with issues of

pain differently. The individual’s own personal and familial history of mental health problems should be explored to include issues of depression, anxiety, problems dealing with reality, and substance use. How the patient may have previously dealt with illness and injury may shed light on their ability to cope or the models for coping they may have witnessed in the past. The individual’s cognitive capacity, level of intellectual functioning, ability to understand the nature of their condition, treatment options, and likely outcomes are important features to understand because they have bearing on how compliant, anxious, depressed, and motivated the individual may be in completing their treatment regimen. Contemporaneous stressors that the person may be experiencing in addition to their injury, illness, or painful condition for which they are being assessed will be important to explore to evaluate how taxed their resources are and also may provide necessary information regarding potential sources of secondary gain that may be promoting abnormal illness behavior. The exploration and history obtained during the psychological clinical interview should likely also provide information about spousal availability or family solicitousness that may be unnecessarily reinforcing pain behaviors. Work history, prior work-related injuries, job changes or losses, and job dissatisfaction are important variables to survey as such factors may be either pressuring and propelling the person toward or repulsing them from relinquishing the disabled role and maintaining symptoms. An awareness of issues involving litigation, finances, and availability of disability compensation can be important to understanding prolonged disability. Other significant pieces of psychosocial history that should be explored include the individual’s educational achievement, military service record, marital or relationship background, legal history, substance use patterns and habits, history of abuse, and available support systems. The pain-related psychological evaluation must adequately cover the full range of issues that have bearing on the individual’s behavior. These will typically include affective disturbances, anxiety disorders, psychotic features, characterologic pathology, somatoform presentations, substance use factors, and magnified or feigned symptoms. Because the expanse of this evaluation casts a broad net, it is not unusual for such an evaluation to be composed of multiple psychological measures.

Screening versus Objective Personality Tests One may also use a stepwise approach to psychologically painrelated evaluation that proceeds from global indices of emotional distress and disturbance to a more detailed evaluation of the most important interactive factors of the diagnosis that may include Axis I clinical disorders and Axis II personality disorders.5 There are two basic types of psychological instruments that can provide useful information when working with pain patients: screening tests and objective personality tests. Some screening tests can assist persons in describing, characterizing, and quantifying pain. Other screening tests can be used to identify conditions that may complicate the course of treatment and need further treatment or evaluation. However, screening tests are typically overly sensitive, are obvious in their intent, and lack validity measures. The advantages of screening tests include: they are inexpensive, quick, and patients typically understand their purpose. Objective personality tests can provide a broader, more detailed evaluation of a patient’s functioning, but they are lengthy and require specialized training to interpret. Objective tests have greater validity and reliability than screening tests.

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16  Basic Principles of Procedures

Pain Rating Scales There are a number of different pain rating scales in use, many of which have been modified for a specific type of clinical setting (orthopedic, rheumatology, oncology, etc.) or specific type of problem (headache scale, neck scale, low back pain scale, etc.). The simplest and most widely used is the Numerical Pain Rating Scale (NPRS) which asks patients to rate their pain from 0 to 10 with 0 indicating no pain and 10 indicating maximum pain.6 In some instances, clinicians will ask the patient to rate their worst pain level and best pain level in the last 30 days, as well as a range of their typical pain level. A pain level of 6 with one patient is not the same as a 6 with another patient because some are more stoic and others more catastrophizing. However, it does allow for some degree of comparison of a single patient over time. Many physicians and therapists will list the Numeric Pain Rating on each contact note to facilitate comparison over time. Visual Analog Scale The Visual Analog Scale (VAS) is a 10 cm line with anchor statements on the left (no pain) and on the right (extreme pain). The patient is asked to mark their current pain level on the line. They can also be asked to mark their maximum, minimum, and average pain. The examiner scores the VAS by measuring the distance in either centimeters (0 to 10) or millimeters (0 to 100) from the “no pain” anchor point. The scores tend to correlate with numerical ratings but some researchers have suggested the Visual Analog Scale is more sensitive to minor changes in pain because it can be measured in millimeters and therefore demonstrate pain changes from 47 to 53, which would both be a 5 on the Numeric Pain Rating scale.7 However, there is no research to support that the Visual Analog Scale is any more accurate when measured in centimeters than it is when it is measured in millimeters nor is there any research on what would represent a reliable change on the VAS. This suggests that the difference in the example between a 47 and 53 is probably not significant and is appropriately viewed as equivalent pain ratings. FACES Pain Rating Scales The Wong-Baker FACES Pain Rating Scale and Faces Pain ScaleRevised (FPS-R) were both developed to assist children in rating pain. They both show six faces in different degrees of distress. The FACES scale starts at 0 with the statement “No Hurt” under a face with a broad smile and continues to 5 with the statement “Hurts worst” and a face with a frown and tears. The FPS-R is similar but the point totals increase in increments of 2 instead of 1 (0 to 10). The FPS-R does not include tears on the faces because they do not want to contaminate the pain rating with an emotional rating. Both scales have been used successfully and are preferred over the NPRS and VAS with children. McGill Pain Questionnaire The McGill Pain Questionnaire (MPQ) is a list of 78 words divided into three domains (Sensory, Affective, and Evaluative) and 6 words for current pain intensity. While the validity of the domains and the MPQ has been called into question by some researchers it continues to be one of the most extensively used pain measures in research and clinical practice. While the quantitative value of the McGill is open for debate the qualitative value is clear. Melzack identified and organized the lexicon of pain in a manner that made it accessible to patients and professionals. Within the three domains are a total to 20 subcategories each containing from 3 to 6 descriptive words. The first domain (sensory) containing subcategories 1 to

10 includes 42 descriptors; the second domain (affective) containing subcategories 11 to 15 includes 14 descriptors; the third domain (evaluative) containing subcategory 16 includes 5 descriptors; and subcategories 17 to 20 are miscellaneous items that contain 17 descriptors. Each subcategory receives a numeric score equal to the rank order of the highest descriptor chosen. For example subcategory 1 includes the following words with the numeric value in parentheses: Flickering (1), quivering (2), pulsing (3), throbbing (4), beating (5), and pounding (6). Subcategory 2 includes the following words with the numeric value in parentheses: Jumping (1), flashing (2), and shooting (3). If the patient identifies “pulsing” and “shooting” each subcategory would have a numerical value of 3 despite “pulsing” being the third of six choices and “shooting” being the third of three choices. The subjective ordinal nature and varied number of items in the subcategories decreases the psychometric soundness of the MPQ. Likewise, the sensory domain has a range of scores from 0 to 42, the affective domain has a range of scores from 0 to 14, the evaluative domain has a range of scores from 0 to 5, and the miscellaneous items can account for 0 to 17 points. As a result of the varied relative contribution of each domain they are not able to be directly compared in a quantitative manner. The domains and miscellaneous items are summed to determine the Pain Rating Index (PRI) and another set of 6 descriptors is provided to identify the Present Pain Index (PPI). Despite the statistical limitations of the MPQ the Pain Rating Index (PRI) and Present Pain Index (PPI) do appear to have high clinical and research utility. They can provide an ipsative comparison for each patient in a test-retest format and allow for a quick point of reference on each patient contact if the PPI is used alone. The descriptors provide an inclusive lexicon of pain quality which makes communication between patient and clinician more accurate and can aid with identifying pain etiology. However, the complexity of the terms can be a problem for patients of lower IQ and other measures should be used in cases of below average IQ.8 The MPQ short-form is a modified version that provides a brief (2 to 5 minutes) alternative to the MPQ (10 to 15 minutes).9 It consists of 15 descriptive words taken from the MPQ subcategories with a Likert scale of 0 to 3 next to each word. The 15 descriptors consist of 10 words and 1 set of combined descriptors (Hot-Burning) from the Sensory Domain and 2 words and 2 sets of combined descriptors (Tiring-Exhausting and Punishing-Cruel) from the Affective Domain. The possible range of scores is 0 to 45. The MPQ short-form also includes the Present Pain Index (PPI) and a Visual Analog Scale (VAS). The short-form has been shown to have high correlations with the original McGill Pain Scale. Oswestry Low Back Pain Disability Questionnaire The Oswestry Low Back Pain Disability Questionnaire (ODQ)10 is a 60 item patient questionnaire which assesses the amount of restriction pain imposes on 10 domains (Pain Intensity, Personal Care, Lifting, Walking, Sitting, Standing, Sleeping, Sex Life, Social Life, and Traveling).11 The Revised version of the ODQ replaced the domain Sex Life with the domain Changing Degree of Pain. While the test items have an average Flesch-Kincaid Grade Level of 5.3 the instructions are written at a Flesch-Kincaid Grade Level of 11.7. Consequently it is important to read the instructions to patients with limited reading skills and to make sure they understand the instructions. Both versions are administered and scored the same way. The patient is asked to identify which of six statements in each domain applies to them at the time of evaluation. The sentences are arranged from no impairment (0) to maximum impairment (5). The scores for each domain are added together (range from 0 to 50)

Psychological Aspects of Pain  17

and multiplied by 2 which yields a Disability Index Score percent. If not all items are completed, the score is prorated by averaging the items completed and then multiplying it by 10. A Disability Index Score of 0% to 20% equals minimal disability, 21% to 40% equals moderate disability, 41% to 60% equals severe disability, 61% to 80% equals crippled, and 81% to 100% indicates a patient that is either bed-bound or exaggerating their symptoms. Scores greater than 40% suggest a more detailed investigation is warranted.

Other Screening Tests Screening tests that are helpful in dealing with patients with painrelated disorders include not only those that directly address pain but also those that screen for conditions that frequently co-occur in pain patients or can complicate the patent’s course of treatment. This can include mood disorders, anxiety disorders, personality traits, and substance-related disorders. Beck Depression Inventory Common screening tests of depression include the Beck Depression Inventory (BDI), Zung Self-Rating Depression Scale (SDS), and Hamilton Depression Rating Scale (HAMD). The Beck Depression Inventory has been used since 1961 and is the most common depression screening instrument. The second edition was published in 1996 (BDI-II) and represents a revision that is more consistent with current diagnostic criteria for depression. The BDI-II consists of 21 items, for example, sadness, pessimism, worthlessness. All items, except two, have four statements of increasing intensity within the domain. For example under sadness the items start with “I do not feel sad.” and end with “I am so sad or unhappy I can’t stand it.” The first item has a score of 0 while the fourth item has a score of 3. The two items evaluating changes in sleeping patterns and changes in appetite have seven total statements, one with a value of 0 indicating no change and two items each for values 1, 2, and 3 indicating mild, moderate, and severe problems (both decreased and increased sleep and decreased and increased appetite). The range of possible scores is 0 to 63. BDI-II scores are classified as minimal (0-13), mild (14-19), moderate (20-28), and severe (29-63).11,12 The strength of the BDI-II is the ease of use, wide age range (13 years and older), low reading level (average Flesch-Kincaid Grade Level 3.6), and substantial body of research. The weaknesses of the BDI-II are typical in screening measures: no validity scales and high face validity allows persons to easily manipulate the total score. Zung Self-Rating Depression Scale The Zung Self-Rating Depression Scale (SDS) consists of 20 items with a Likert type scale after each item. The scores for each item range from 1 to 4 and the SDS ranges from a raw score of 20 to a raw score of 80. Some items are reverse scored (i.e., they go from 4 down to 1). It has not been as well researched as the BDI-II but has been used in clinical trials of antidepressant medications. It was developed in 1965 and had not been updated. The reading level is even lower than the BDI-II (average Flesch-Kincaid Grade Level 2.2). SDS scores are classified as normal (<50), mild depression (50 to 59), moderate to marked major depression (60 to 69), and severe to extreme major depression (>70). The raw score can be converted to an SDS Index score by multiplying the raw score times 1.25. Hamilton Depression Rating Scale The Hamilton Depression Rating Scale (HAMD) is completed by the clinician as opposed to the patient. It consists of 17 items with Likert scale of either 0 to 4 or 0 to 2. Scores can range from 0 to 54.

The HAMD was developed in 1957 and has been used extensively within the medical community but is not typically used by psychologists. HAMD scores correlate well with BDI-II scores and can be used in place of a self-report when a patient is unable to read. It can also be used when there are concerns about the accuracy of the patient’s self-report. HAMD scores are classified as normal (<9), mild depression (10 to 13), mild to moderate depression (14 to 17), and moderate to severe depression (>17). Beck Anxiety Inventory The Beck Anxiety Inventory (BAI) consists of 21 items with a Likert scale ranging from 0 to 3 and raw scores ranging from 0 to 63. It was developed in 1988 and a revised manual was published in 1993 with some changes in scoring. The BAI scores are classified as minimal anxiety (0 to 7), mild anxiety (8 to 15), moderate anxiety (16 to 25), and severe anxiety (30 to 63). The BAI correlates highly with the BDI-II indicating that although the BAI may provide useful clinical information, it is not specific and can’t be used diagnostically. The reading level is even lower than the BDI-II (average Flesch-Kincaid Grade Level 2.3. Because the instructions for the BAI are written at an 8.3 grade level, oral instructions should be given to persons with lower reading skills. Substance Abuse Subtle Screening Inventory Substance abuse screening tests can provide useful information when working with patients with a history of alcohol or substance abuse. The Substance Abuse Subtle Screening Inventory—Third Edition (SASSI-3) includes a set of obvious items asking about drug use and alcohol use. If the person is unwilling to openly acknowledge excessive alcohol or drug use, there are other scales that can assist in evaluating possible abuse/dependence. The SASSI-3 includes the following scales: Symptoms (SYM), Obvious Attributes (OAT), Subtle Attributes (SAT), Defensiveness (DEF), Supplemental Addiction Measure (SAM), Family versus Control Measure (FAM), Correctional (COR), and Random Answering. The defensiveness and random answering scales are rudimentary validity scales. There is a decision tree that assists with diagnostic impressions.

Objective Personality Tests A more comprehensive evaluation can be completed by a psychologist using objective personality tests. These tests must be interpreted by a psychologist and can provide significant information useful in the diagnosis and treatment of the patient with pain. The most commonly used and thoroughly researched objective personality test is the Minnesota Multiphasic Personality Inventory which is currently in its second edition (MMPI-2). There is also a recently published somewhat shorter restructured form (MMPI2-RF) based on the MMPI-2. The Personality Assessment Inventory (PAI), Millon Clinical Multiaxial Inventory—Third Edition (MCMIIII), and Millon Behavioral Medicine Diagnostic (MBMD) are other less frequently used objective personality measures that can provide valuable information. Minnesota Multiphasic Personality Inventory The MMPI-2 is the most widely used and heavily researched psychological test in the United States. Originally developed in the late 1930s and revised in 1989, it currently consists of 567 true/false questions. The MMPI-2 items make up a number of scales including 10 standard validity scales, 10 clinical scales with 28 subscales, 18 supplemental scales, and 15 content scales. The MMPI-2 can be administered to patients 18 years and older and requires a 6th grade

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reading level. The adolescent version (MMPI-A) is administered to persons 14 to 18 years of age and is similar to the MMPI-2, but is not nearly as well researched. The MMPI-2 is used in medical, psychological, employment, and legal settings. The MMPI-2 is valued as much, if not more, for its validity scales than it is for the clinical information that can be derived from it. The first validity scale addresses the number of items omitted, and is the raw score of items which have not been answered as either true or false. If the patient fails to complete too many items, it may invalidate the profile. The validity scales include measures that evaluate if the patient is nonresponsive to questions. This could be due to acquiescent (yea saying) or counter-acquiescent (nay saying) response sets as measured by the True Response Inconsistency (TRIN) scale. It could also be due to inconsistency between items of similar content as measured by the Variable Response Inconsistency (VRIN) scale. Elevations on either scale could be due to reading problems, motivational problems, or haphazard response sets. In cases of marginal elevations on VRIN, the data are viewed as less reliable and interpretation of elevated scales is more cautious. Validity scales that suggest underreporting of pathology include scales in which a person is trying to present an overly virtuous image (L), a guarded presentation (K), and a highly confident/ competent self-presentation (S). When these underreporting scales are elevated, it typically reflects minimization of symptoms. While this does not typically invalidate the MMPI-2, it can lead to a suppression of symptoms to the point that there are no clinically meaningful elevations on the test. Validity scales that suggest overreporting of pathology include a series of scales that are composed of infrequently endorsed items. These are low base rate items which are primarily vague or nonspecific symptoms. Elevations indicate the patient is endorsing an inordinate number of these low base rate symptoms. These scales include the Infrequency Scale (F), Infrequency Back (Fb), and Infrequency Psychopathology (Fp). The F and Fb are similar scales but F items occur on the first 370 items and include more chronic symptoms, whereas Fb items occur after item 280 and include more acute symptoms. Elevations on the F and/or Fb scale can be due to any or all of the following reasons: (1) random or fixed patterns of responding which would lead to elevations on VRIN and TRIN, respectively; (2) accurate descriptions of severe psychopathology; and (3) purposely overreporting symptoms. While VRIN and TRIN can help rule-out random or fixed patterns of responding, it is more difficult to differentiate between severe psychopathology and purposeful overreporting of symptoms. The Fp scale was developed to assist in this determination. The Fp scale is composed of low base rate symptoms in an inpatient psychiatric population. The Fp scale is less sensitive than F to the presence of severe psychopathology. The Fake Bad Scale (FBS) is described as having been devised to detect a model of goal directed behavior with a focus on appearing to be honest; appearing psychologically normal, except for the influence of the alleged cause of injury; avoiding admitting to preexisting psychopathology; where preexisting complaints are known, or suspected to have been disclosed to the examining clinician, attempting to minimize those complaints; hiding preinjury behaviors that are antisocial, illegal, or minimizing it if it appears the behaviors will be discovered independently; and presenting an extent of injury or disability within a perceived limit of plausibility (Lees-Haley, English, Glenn, 1991). The FBS continues to be a controversial scale, but the publisher of the MMPI-2 has recognized the FBS as a reported scale and includes it in the standard MMPI-2 report. By using the more conservative cutoffs of raw scores

(24 for males and 26 for females) the concern of a high false-positive rate has been minimized. The existent literature indicates that raw scores above 28 on the FBS are associated with a very low falsepositive rate.13 Additionally, the literature suggests that increasing confidence is placed in scores as they rise above a cutoff of 30, with a number of studies noting that no nonlitigant, nonmalingering subjects had raw scores of 30 or above.14 There are a number of less commonly used validity scales that are used by some researchers and clinicians. One particularly interesting additional validity scale is the Meyers Validity in Chronic Pain Index (Meyers Index) that uses a chronic pain population.15 The developers combined seven different validity scales on the MMPI-2 into a common weighted method in assessing malingering in chronic pain patients. This weighted method was able to correctly classify 100% of nonlitigants using a cutoff score of equal to or greater than 5. That study suggested chronic pain patients in litigation produce a different profile on the MMPI-2 validity scales than do nonlitigants. The Meyers Index is calculated by assigning values of 0, 1, or 2 on seven validity scales based on the level of elevation on each scale. The Meyers Index score is classified as okay (0 to 2), exaggerated (3 to 4), malingered (5 to 8), and clearly malingered (9 to 14). The Meyers Index uses the following scales (F, FBS, F-K, Fp, Ds-r, Es, and O-S). Once an MMPI-2 profile has been determined to be valid, the Clinical Scales and Subscales can be evaluated to provide information about the patient’s psychological and emotional functioning. The MMPI-2 retained the same 10 MMPI clinical scales including the scale names and numbers. Some of the scale names are antiquated (e.g., Psychasthenia) and as such are typically referred to by number or abbreviation. For example scale 2 is Depression and is generally called scale 2 or the D scale. The Clinical Scales were initially developed using a method known as empirical criterion keying and as such are not based on any specific theory or diagnostic criteria. Each clinical scale is a combination of items that a specific group (e.g., depressed patients) answered differently than the comparison group. The fact that the MMPI-2 is not tied to a diagnostic system such as the DSM or ICD is an advantage and disadvantage. The advantage is the MMPI-2 does not change each time the diagnostic criteria are changed. This allows for comparison of MMPI-2 profiles across time and facilities research. The disadvantage is that the MMPI-2 does not provide and lend itself well alone to making a DSM diagnosis. For example, an elevation on scale 2, the Depression scale, does not indicate the presence of major depression. It could be depressive symptoms due to dysthymic disorder, grief, or depressive symptoms due to recent emotional stressors such as a severe work-related injury to a patient’s spouse. Consequently the MMPI-2 cannot be interpreted effectively in a vacuum and “blind interpretation” of the MMPI-2 tends to lead to interpretive statements which include a substantial amount of error within the interpretive statements. This suggests great care needs to be taken in dealing with blind, computer-generated interpretive reports. Interpretation of profiles from medical patients using a psychological or psychiatric comparison group can lead to erroneous interpretations and misdiagnosis. Consider, for example, compiled MMPI-2 norms for a chronic pain population using 209 chronic pain inpatients.16 The chronic pain patients scored significantly higher than controls on 9 of the 10 clinical scales. Traditional interpretive methods would over-pathologize the patients with chronic pain. Clinical Scales 1, 2, and 3 are the most frequently elevated scales in a chronic pain population. The typical chronic pain profile will present a “conversion V” or somatic profile. If these scales are

Psychological Aspects of Pain  19

elevated when compared with a chronic pain reference group then a somatization or conversion disorder may be present. In addition to the Clinical Scales there are a number of other scales on the MMPI-2. Although these are less heavily researched than the Clinical Scales, they can still provide useful information. Additional scales include the Content Scales, Supplemental Scales, and Restructured Clinical Scales. The Content Scales include the following scales: Anxiety, Fears, Obsessiveness, Depression, Health Concerns, Bizarre Mentation, Anger, Cynicism, Antisocial Practices, Type A, Low Self-Esteem, Social Discomfort, Family Problems, Work Interference, and Negative Treatment Indicators. The Supplemental Scales include the following scales: Anxiety, Repression, Overcontrol-Hostility, Dominance, Ego Strength, Social Responsibility, College Maladjustment, MacAndrew Alcoholism-Revised, Addiction Admission, Addiction Potential, Marital Distress, PTSD, Gender Role—Masculine, and Gender Role—Feminine. The Content and Supplemental Scales are labeled using more contemporary labels, which typically do not require additional explanation. MMPI-2 Restructured Form The Restructured Clinical Scales are relatively new scales that show promise, but have not been fully evaluated in pain patients. The Restructured Clinical Scales also form the core of a new version of the MMPI-2 which is called the MMPI-2 Restructured Form (MMPI-2-RF). The MMPI-2-RF retains many of the positive features of the MMPI-2 in a shorter format, 338 items versus the 567 items of the MMPI-2. The MMPI-2-RF includes revised versions of many of the MMPI-2 validity scales, but does not include the traditional Clinical Scales. There a several promising aspects to the new MMPI-2-RF including a new validity scale that assesses for the presence of Infrequent Somatic Responses (Fs). There are also a number of problemspecific scales that focus on Somatic/Cognitive Dysfunction. Personality Assessment Inventory The Personality Assessment Inventory (PAI) is another objective personality measure. It is composed of 344 items with 4 possible responses for each item (False, Slightly True, Mainly True, and Very True). It consists of 22 scales including 4 validity scales, 11 clinical scales, 5 treatment consideration scales, and 2 interpersonal scales. The reading level (average Flesch-Kincaid Grade Level 4.1) is lower than the MMPI-2. There has been some research using the PAI in chronic pain settings that should increase the utility of the test.17 The PAI addresses psychological disorders, personality disorders, and substance abuse disorders making it a very high utility test and an acceptable alternative to the MMPI-2 in some settings. The validity scales are not as well researched as the MMPI-2, which limits its use in medicolegal settings unless used in conjunction with other symptom validity tests. Millon Clinical Multiaxial Inventory—Third Edition The Millon Clinical Multiaxial Inventory—Third Edition (MCMIIII) is another frequently used objective personality measure. The MCMI-III provides information about the presence of psychological disorders including personality disorders. The MCMI-III is a 175-question, true/false psychological instrument used in clinical settings with individuals 18 years and older. The reading level (average Flesch-Kincaid Grade Level 5.7) is higher than the MMPI-2. The normative population is composed of patients seen in individual practice, clinics, mental health centers, forensic settings, residential facilities, and hospitals. The MCMI-III uses “Base Rate” scores for the purposes of reporting and interpretation. A Base Rate

(BR) score of 60 [BR60] represents the median score, as opposed to T scores where 50T is the median, with BR0 being the lowest possible score and BR115 the highest. The presence of a specific personality trait is generally indicated at BR75, whereas scores of BR85 and above suggests the full presence of a personality characteristic. Base rate scores are criterion, not norm, referenced—indicating that BR scores do not indicate if a score is common or not, only whether the trait or characteristic is present. The MCMI-III has 28 scales including 14 Personality Disorder Scales, 10 Clinical Syndrome Scales, 4 Correctional Scales. The Personality Disorder Scales include: Schizoid, Avoidant, Depressive, Dependent, Histrionic, Narcissistic, Antisocial, Sadistic (Aggressive), Compulsive, Negativistic (Passive-Aggressive), Masochistic (Self-Defeating), Schizotypal, Borderline, and Paranoid. The Clinical Syndrome Scales include: Anxiety, Somatoform, Bipolar, Manic, Dysthymia, Alcohol Dependence, Drug Dependence, Post-Traumatic Stress Disorder, Thought Disorder, Major Depression, and Delusional Disorder. The Correctional Scales include: Disclosure, Desirability, Debasement, and Validity. The Personality Disorder Scales were designed to correlate with DSM-IV Axis II disorders, whereas the Clinical Syndrome Scales correlate with the DSM-IV Axis I disorders. Another study examined the ability of the MCMI-III to be reliably used to assess intervention in pain management at a pain management center in Paducah, Kentucky.18 One hundred consecutive patients were evaluated for major depression or generalized anxiety disorder using a DSM-IV-TR questionnaire and physician interview; all participants also completed the MCMI-III and P-3 inventories as part of a psychological evaluation. A positive diagnosis of major depression or generalized anxiety disorder, using the DSM-IV-TR criteria, was considered the criterion standard. The diagnosis of major depression on the MCMI-III showed 100% specificity but only 54% sensitivity; for generalized anxiety disorder, the MCMI-III specificity was 89%, whereas the sensitivity was 73%. Millon Behavioral Medicine Diagnostic The Millon Behavioral Medicine Diagnostic (MBMD) is a revised version of the Millon Behavioral Health Inventory (MBHI) and was designed to provide helpful information on a patients’ biopsychosocial health. The test aids in recommending potential treatment strategies and may help in proactively identifying potential pitfalls to treatment. The MBMD can be used with individuals 18 years to 89 years and requires a sixth grade reading level. Consisting of 165 true/false questions, the MBMD typically takes 20 to 25 minutes to complete. The MBMD allows the clinician to select one of two normative samples—a general medical sample and a sample of prescreened bariatric surgery patients. The MBMD consists of 29 content scales, grouped into five domains, six negative health habits, and three scales to detect response patterns. The Content Scales include the following: 5 Psychiatric Indicators (Anxiety-Tension, Depression, Cognitive Dysfunction, Emotional Liability, and Guardedness); 11 Coping Styles (Introverted, Inhibited, Dejected, Cooperative, Sociable, Confident, Non-Conforming, Forceful, Respectful, Oppositional, and Denigrated); 6 Stress Moderators (Illness Apprehension, Functional Deficits, Pain Sensitivity, Social Isolation, Future Pessimism, and Spiritual Absence), 5 Treatment Prognostics (Interventional Fragility, Medication Abuse, Information Discomfort, Utilization Excess, and Problematic Compliance), and 2 Management Guides (Adjustment Difficulties, and Psych Referral). There are 6 Negative Health Habits (Alcohol, Drugs, Eating, Caffeine, Inactivity, and Smoking). There are 3 Response Patterns (Disclosure, Desirability, and Debasement).

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Despite the success of the MBMD in assessing biopsychosocial health characteristics and treatment options, practitioners have been warned to be cautious when using the MBMD because limitations in clinical use may arise in specific populations.19

Psychotherapy In recent decades, studies evaluating the use of psychotherapy as a treatment option in patients with pain have significantly increased. Physicians, psychologists, and patients have become increasingly aware of mind-body connections and the utility of treating the psychological conditions that may both exacerbate, and result from, chronic pain. A variety of treatment models are available to the mental health professional to help patients manage symptoms and intensity, deal with the functional limitations that chronic pain may place on their lives, gain realistic expectations and coping skills, and be able to deal with any other preexisting psychological conditions that could hamper positive therapy outcomes. In the treatment of the individual with pain, the therapist needs to address the patient’s expectations for treatment, not only to ensure that their expectations are realistic and achievable, but to offer hope to patients who may feel marginalized and distressed. One study involving three groups of people referred to a pain management clinic found that in all three groups, the persons referred described experiencing feelings of embarrassment, frustration, and lack of self-control.20 The patients also reported they often felt others did not believe their pain and viewed physicians as attempting to “fob them off ” by prescribing pain medication. A primary goal during the initial intake process and first sessions is to normalize the experience of patients’ emotions and assist them in establishing reasonable treatment expectations. As such, no “cure” that will allow the patient to be pain-free can be guaranteed, but a treatment plan can be developed in collaboration with the patient that will address the patient’s specific concerns and help them to better manage their pain symptoms and any associated psychopathology. It is important for the therapist to understand how the experience of pain has altered or affected the patient’s activities of daily living, occupational and social functioning, affect and mood, and family relationships. Treatment approaches can be tailored to the variety found among chronic pain patients and evidence-based practice allows for adaptation to meet the needs of the individual patient. As discussed, the importance of assessing variables that may influence or mediate the patient’s experience of pain, personality characteristics, or preexisting psychological pathology or conditions may have a significant bearing on the nature and direction of the therapeutic process.21-23 The treatment models discussed in this chapter are by no means an exhaustive list; they instead highlight methods that are research-based approaches and are broad enough to be used in a variety of contexts.

Cognitive—Behavioral Therapy The most widely acclaimed and researched approach to psychological pain management is cognitive-behavioral therapy (CBT). Both cognitive and behavioral interventions to treat chronic pain have considerable empirical support.24 A metaanalysis of 25 randomized controlled trials of CBT for pain management revealed CBT to produce “significantly greater changes for the domains of the pain experience, cognitive coping and appraisal (positive coping

measures), and reduced behavioral expression of pain when compared with alternative active treatments.”24 CBT emphasizes changing maladaptive patterns of thinking and feeling in response to the pain, and encompasses a wide range of strategies, including relaxation training, cognitive restructuring/reframing, distraction techniques, and stress management; goal-setting is also highlighted. Additionally, this treatment model can be used in individual or group settings, relies heavily on therapist-patient collaboration, and is considered an optimistic approach to pain management because it teaches the sufferer that his or her experience of pain can be mediated by changing his or her maladaptive beliefs.25 For example, the therapist may teach relaxation techniques, challenge irrational beliefs and cognitive errors (such as thinking of themselves as helpless or their situation as hopeless), and place behaviors within the patient’s locus of control. CBT posits behavior as voluntary and not controlled by external events, and thus may offer the patient alternative courses of action. Patient catastrophizing (i.e., a process of exaggerated worrying, acute distress, and helplessness in response to pain) has also been found to occur with consistent regularity among patients with chronic pain.26 Restructuring the patients’ thoughts via cognitivetype therapy helped the patients to accept their pain and mediated the catastrophizing effects of pain when applied to such variables as depression, pain-related fear, and disability. It was concluded that although helping patients accept and not catastrophize pain did not lessen pain intensity, it did help these patients improve overall functioning and emotional well-being.26 Although CBT may be considered the ‘gold standard’ for psychotherapy, research findings have substantial variability among outcome measures and invite speculation regarding the overall efficacy of CBT.23 It therefore behooves clinicians to be familiar with other evidence-based approaches to tailor therapy to suit the needs of individual patients. Other such approaches include Coping Skills Development (CSD), Integrated Psychosocial-Spiritual Models, and mindfulness meditation. These may be used as singular interventions or in conjunction with other types of therapy.

Coping Skills Development The CSD program is a “biopsychosocial model with emphasis on learning general coping skills primarily and pain coping skills secondarily.”24 The overall goal of the program was to help the patients develop an internal locus of control through teaching and helping patients integrate four basic coping skills: self-determination, selfesteem, feelings, and exercise. Although CSD differs from CBT in that it has a broader focus (for example, CSD examines the roles of self-esteem and emotions), there is a definitive cognitive component of CSD that is quite similar to CBT: CSD rests on the premise that “people who think rationally and take responsibility for what they think and do, have good self-esteem, and recognize their true feelings and express them in reasonable ways can cope well despite most trying circumstances including chronic pain”24 This hypothesis appears to be supported: post-treatment results indicated less pain severity, less pain interference, more life control, decreased levels of depression, and more hours of activity per day. At 1-year follow-up, there remained an overall decrease in the use of prescription narcotic medication, as well as fewer health care visits, indicating that the patients were better able to manage their pain with less dependence on medication and physicians. Additionally, the percentage of persons in work or in training had increased, and those on compensation had decreased. It is noteworthy, however,

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that this treatment was administered in a group format; there are no outcome studies for this approach when used in individual therapy.

Integrated Psychosocial—Spiritual Model The Integrated Psychosocial-Spiritual Model was developed to manage cancer pain, and argues that a complex, multidimensional treatment approach is necessary to effectively treat a complex, multidimensional problem such as cancer pain.27 This model adopts a holistic approach, addressing several aspects of pain, including emotions, cognitions, social factors, behaviors, and spiritual concerns. The authors contend that each of these factors is influenced by pain, and all must be treated or addressed to create a robust therapeutic outcome.

Mindfulness Meditation Mindfulness meditation is yet another treatment approach that can be successful for the patient with chronic pain. Mindfulness meditation promotes strategies that support emotional regulation through awareness of, and change in, dysfunctional thoughts. It also enhances positive emotions through awareness of positive states, a piece missing from traditional CBT. This model specifically targets the patient’s ability to relate differently to the thoughts and feelings associated with periods of negative affect, and to interrupt the automatic responding that often occurs in these states. Researchers who use this model have been able to highlight the necessity of assessing and considering preexisting psychological conditions that may influence therapy outcomes. For example, one study compared the efficacy of CBT and mindfulness meditation in treating patients with rheumatoid arthritis (RA).21 The researchers assessed history of recurrent depression, formed groups based on this variable, and then assigned these groups to one of three treatment methods: mindfulness-based emotion regulation therapeutic program (aimed at promoting awareness and change of meaning given to dysfunctional thoughts), CBT, or an education group that served as the control. They measured several outcome variables, including daily pain, positive and negative affect, depressive symptoms, coping efficacy for pain, pain catastrophizing, and pain control. The patients also submitted to physician assessments of joint-tenderness and provided blood samples to measure the production of IL-6 (the proinflammatory cytokine that is associated with joint destruction in RA patients). The outcome results revealed both of the methodologies (mindfulness meditation and CBT) to be useful, but in different ways. In this case, the mindfulness meditation approach proved to be more useful for those with a history of chronic depression, whereas CBT had better outcomes for those without a history of recurrent depression. For the recurrent depression group, the mindfulness intervention made a greater difference in reducing the perception of pain and enhancing positive affect.

Influence of Personality Factors Personality factors can be another important therapeutic consideration in the treatment of patients with pain. Correlations between personality and therapy satisfaction support the notion that treatment satisfaction may be an important predictor of outcome for medical and psychological treatments, including chronic pain.25 In using the NEO Five Factor Inventory and brief CBT, researchers found that “the core personality dimensions of neuroticism, openness, and agreeableness were predictive of aspects of satisfaction

with therapy.”23 Specifically, neuroticism negatively affected treatment satisfaction; whereas agreeableness had a statistically significant correlation with the individual viewing the therapy sessions as running smoothly (agreeable individuals are also more likely to participate in specific therapy components, such as ‘homework assignments’). Patients scoring higher on the Openness dimension tended to evaluate the sessions as having less depth, although the researchers believed this may have been due to these patients being more willing to participate in in-depth exploration, which was not available in the brief therapy format used in this study. Perhaps longer interventions might provide the depth these patients appear to seek. This study is also helpful because it highlights the effect of variables outside of the chronic pain itself that may influence therapy outcomes. It adds to the argument that treatment selection should meet the needs of the individual patients, which includes an assessment and integration of specific characteristics, including preexisting pathology and personality.

Modes of Therapy When considering treatment, clinicians have the option of several modes of therapy, including group, individual, long-term, or brief. Group therapy is well supported in the literature and offers many advantages that may not be available in individual therapy.28-30 These include helping to disconfirm common pain myths, giving members a sense of community and universality (thus, decreasing one’s sense of alienation and isolation), promoting shared catharsis, and providing members a forum in which to offer personal skills and pain management techniques.31 Not all patients will be suitable for group therapy, either due to personality or if the patient issues are beyond the goals of the group.30 Clinicians should screen patients for group in order to determine suitability, as well as be willing to transfer group members to individual therapy, when appropriate.

Family Considerations It is logical that individuals with pain do not experience their pain in a relational vacuum and it is often helpful to understand the patient within the family context because the family shapes and is shaped by the transactional patterns of the family system.32 Families, spouses, and friends are potentially affected as they may have questions as to how to help their loved one, and have to cope with possible role changes within the relationship. The patient with pain may require financial, emotional, and personal care. Clinicians must decide in collaboration with the patient, whether, and to what extent, to include family members in treatment. In some cases, family members will need to be brought into the therapy process because they may be unwittingly reinforcing abnormal illness behavior by being overly solicitous or sometimes a lack of emotional support and encouragement may be resulting in the patient feeling alone, alienated, rejected, and/or depressed. In such cases, if appropriate family members are not part of the treatment they may maintain or perpetuate the problems of the chronic pain sufferer.31

Conclusion As can be seen, the psychological assessment and treatment of pain is a complex, multidimensional process. The consulting psychologist can often provide useful information to the treating physician

3

22  Basic Principles of Procedures

or augment medical treatment through the use of effective psychological assessment techniques and appropriate psychotherapy. Depending on the context of the referral, the role of the psychological clinician may include helping patients delineate the psychological aspects of their pain, dealing with family and emotional issues, and providing a sense of self-efficacy that goes beyond pain reduction. Such assessment and intervention may not only lead to a lessening of pain perception, but may also provide the patient a set of tools to function more fully, enjoy a better quality of life, and reach their highest level of functioning possible despite pain. REFERENCES   1. Melzack R, Wall PD. Pain mechanisms: A new theory. Science. 1965;50:971-979.   2. Turk DC, Monarch ES. Biopsychosocial Perspective on Chronic Pain. In: Turk DC, Gatchel RJ, eds. Psychological Approaches to Pain Management: A Practitioner’s Handbook. 2nd ed. New York: Guilford Press; 2002:1-29.   3. Loeser JD. Concepts of pain. In: Stanton-Hicks J, Boaz R, eds. Chronic Low Back Pain. New York: Raven Press; 1982:145-148.   4. Ownby RL. Psychological Reports: A Guide to Report Writing in Professional Psychology. 3rd ed. New York: John Wiley and Sons; 1997.   5. Gatchel RJ. Clinical Essentials of Pain Management. Washington, DC, American Psychological Association; 2005.   6. King S. The classification and assessment of pain. International Review of Psychiatry. 2000;12:86-90.   7. Kahl C, Cleland JA. Visual Analogue Scale, Numeric Pain Rating Scale, and the McGill Pain Questionnaire: An overview of psychometric properties. Physical Therapy Review. 2005;10:123-128.   8. Melzack R. The McGill Pain Questionnaire. In: Plake BS, Impara JC, eds. The Fourteenth Mental Measurements Yearbook. Lincoln University, University of Nebraska Press; 2001.   9. Melzack R. The short-form McGill Pain Questionnaire. Pain. 1987; 30:191-197. 10. Fairbank JC, Couper J, Davies JB, O’Brien JP. The Oswestry low back pain disability questionnaire. Physiotherapy. 1980;66:271-273. 11. Gonzales VA, Martelli MF, Baker JM. Psychological assessment of ­persons with chronic pain. NeuroRehabilitation. 2000;14:69-83. 12. Beck AT, Steer RA, Brown GK. BDI-II Manual. San Antonio, TX: The Psychological Corporation; 1996. 13. Ben-Porath Y, Tellegan A: MMPI-2 FBS (Symptom Validity Scale). Retrieved from Pearson Assessments for Clinical and Psychological Use, 2007. 14. Larrabee GJ. Assessment of malingering. In: Larrabee GJ, ed. Forensic Neuropsychology. New York: Oxford University Press; 2005. 15. Meyers JE, Millis SR, Volkert K. A validity index for the MMPI-2. Arch Clin Neuropsychol. 2002;17:157-169. 16. Slesinger D, Archer RP, Duane, W: MMPI-2 characteristics in a chronic pain population. Assessment. 2002;9:406-414.

17. Karlin BE, Creech SK, Grimes JS, et al. The Personality Assessment Inventory with chronic pain patients: Psychometric properties and clinical utility. J Clin Psychol. 2005;61:1571-1585. 18. Rivera JJ, Singh V, Fellows B, et al. Reliability of psychological evaluation in chronic pain in an interventional pain management setting. Pain Physician. 2005;8:375-383. 19. Walfish S, Wise EA, Streiner DL. Limitations of the Millon Behavioral Medicine Diagnostic (MBMD) with bariatric surgical candidates. Obes Surg. 2008;18:1318-1322. 20. Allcock N, Elkan R, Williams J. Patients referred to a pain management clinic: Beliefs, expectations, and priorities. J Adv Nurs. 2007;60: 248-256. 21. Zautra AJ, Davis MC, Reich JW, et al. Comparison of cognitive behavioral and mindfulness meditation interventions on adaptation to rheumatoid arthritis for patients with and without history of recurrent depression. J Consult Clin Psychol. 2008;76:408-421. 22. Cole JD. Psychotherapy with the chronic pain client using coping skills development: Outcome study. J Occup Health Psychol. 1998;3: 217-226. 23. Green SM, Hadjistavropoulos T, Sharpe D. Client personality characteristics predict satisfaction with cognitive behavior therapy. J Clin ­Psychol. 2008;64:40-51. 24. Otis JD. Managing chronic pain: A cognitive-behavioral therapy approach. New York: Oxford University Press; 2007. 25. Holzman AD, Turk DC, Kerns RD. The cognitive-behavioral approach to the management of chronic pain. In: Holzman AD, Turk DC, eds. Pain management. Elmsford, New York: Pergamon Press; 1986:31-50. 26. Vowles KE, McCracken LM, Eccleston C. Patient functioning and catastrophizing in chronic pain: The mediating effects of acceptance. Health Psychol. 2008;27(suppl 2):S136-S143. 27. Otis-Green S, Sherman R, Perez M, Baird RP. An integrated psychosocial-spiritual model for cancer pain management. Cancer Pract. 2002; 10 (suppl 1):S58-S65. 28. Mannerkorpi K, Gard G. Physiotherapy group treatment for patients with fibromyalgia—an embodied learning process. Disabil Rehabil. 2003;25:1372-1380. 29. Bogart RK, McDaniel RJ, Dunn WJ, et al. Efficacy of group cognitive behavior therapy for the treatment of masticatory myosascial pain. Military Medicine. 2007;172:169-174. 30. Yalom I. The theory and practice of group psychotherapy. 3rd ed. New York: Basic Books; 1985: 1-16. 31. Gentry WD, Owens D. Pain groups. In: Holzman AD, Turk DC, eds. Pain management. Elmsford, New York: Pergamon Press; 1986. 32. Roy R. A problem-centered family systems approach in treating chronic pain. In: Holzman AD, Turck DC, eds. Pain management. Elmsford, New York: Pergamon Press; 1986:113-130. 33. Lewandowski W, Morris R, Draucker CB, Risko J. Chronic pain and the family: Theory-driven treatment approaches. Issues Ment Health Nurs. 2007;28:1019-1044.

Conscious Sedation for ­Interventional Pain Procedures

4

Michael S. Leong, MD, and Steven H. Richeimer, MD Conscious sedation and analgesia are often overlooked aspects of interventional pain procedures. Patients expect to be comfortable during their injections. Physicians tend to concentrate more on the procedure with the sedation becoming secondary. However, when the procedure is not going smoothly, oversedation and analgesia can add problems, such as interpreting paresthesias, intraneural injections, and even loss of airway reflexes—particularly problematic at outpatient surgery centers where airway specialists may not be available. The authors of this chapter are board-certified anesthesiologists and pain medicine specialists. It may be interesting to note that the optimal sedation and analgesia seems to be the least amount possible! One of the caveats of anesthesia training is that sedation and analgesia can always be titrated to effect for the individual patient. Although anesthesiologists can induce the full spectrum of sedation including general anesthesia, most elective pain procedures require far less. The following chapter is for safety guidelines and recommendations and not a “cookbook” on set dosages for sedation and analgesia. Appropriate preparation of the patient, procedural facility, medical support teams, and physicians with procedural techniques can make the scheduled interventions safe and relatively “pain-free” for everyone involved.

Conscious Sedation Conscious sedation is an older term from 1985 to describe lightly sedated dental patients.1 It is defined as the sedation depth that permits appropriate response to physical stimulation or verbal command (e.g., “open your eyes”). Many groups, including the American Association of Anesthesiology and American College of Emergency Physicians believe that the term conscious sedation is imprecise and they propose terms such as sedation/analgesia2 or procedural sedation and analgesia (PSAA),1 or monitored anesthesia care (MAC).3 Indeed, in the first ASA guidelines from February 1996, a notable comment is that patients whose only response is reflex withdrawal from a painful stimulus are sedated to a greater degree than encompassed by sedation/analgesia. A continuum of depth of sedation was described in the second ASA guidelines for sedation/analgesia.4 From Table 4-1, concepts ranging from minimal sedation (anxiolysis) through moderate sedation/analgesia (conscious sedation) to general anesthesia are described related to responsiveness and airway management. Of note, moderate sedation/analgesia is described as purposeful response to verbal or tactile stimulation and that no airway

intervention is required. A more detailed sedation continuum (Table 4-1) is proposed in a Canadian Emergency Department consensus guideline.5 However, the transition between moderate sedation and deep sedation where airway management is required can be different with each patient. The best approach is to establish a sedation/analgesia plan prior to starting the procedure. Optimal goals include the following6: 1. To provide adequate analgesia, sedation, anxiolysis, and amnesia during the performance of painful diagnostic or therapeutic procedures 2. To control unwanted motor behavior that inhibits the performance of diagnostic procedures or image-guided interventions 3. To rapidly return the patient to a state of consciousness 4. To minimize the risks of adverse events related to the provision of sedation and analgesia In addition, the complexity and duration of the procedure involved changes the sedation/analgesia plan. Simple and short procedures may require little or no sedation with only local or topical analgesia, such as trigger point injections or piriformis muscle injections. Many procedures requiring fluoroscopic guidance can be assisted with moderate sedation including midazolam and fentanyl. Although some interventional pain experts routinely perform medial branch blocks under local analgesia only, multiplelevel procedures versus single-level procedures may require more than midazolam 2 mg and fentanyl 100 mcg IV, particularly at a training institution. Cancer neurolytic blocks that can be intensely stimulating often require deeper sedation. Prolonged sedation may be required for spinal cord stimulation trials or intrathecal catheter implants due to the duration of the procedure (see Table 4-1). Physician preparation and experience can decrease the duration of the procedure, thereby decreasing the need for sedation and analgesia.

Patient Preparation One of the main ways of decreasing sedation and analgesia requirements is to prepare patients for what happens during the procedure and hence reducing their anxiety of the unknown. It is easiest for those patients who are returning for a series of the same procedure. Short procedural materials or websites describing the procedure can help patients with questions in the office or preoperative area. Although the literature is insufficient in supporting preprocedural preparation, the ASA consultants agree that “appropriate preprocedure counseling of patients regarding risks, benefits, and alternatives to sedation and analgesia increases patient satisfaction.”4 23

24  Basic Principles of Procedures

Table 4-1  Depth of Sedation and Type of Interventional Procedure Area

Minimal Sedation

Moderate Sedation

Deeper Sedation

Cervical

Occipital block, stellate block

Cervical medial branch blocks, ­cervical epidural

Cervical discogram

General Anesthesia

Thoracic

Intercostal block

Thoracic facet and transforaminal epidurals

Thoracic sympathectomy, thoracic discogram

Spinal cord stimulator implant (after location is verified)

Lumbar

Lumbar psoas block

Lumbar sympathetic, median branch, ­transforaminal epidurals

Celiac plexus block, lumbar discograms

Intraspinal pump placement (after catheter placement)

Sacral

Piriformis block, sacroiliac joint injection

Sacral nerve root blocks, impar ­ganglion block

Superior hypogastric plexus block, epiduroscopy

From American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by ­non-anesthesiologists. Anesthesiology 2002;96:1004-1017.

Table 4-2  ASA Classification

Table 4-3  Summary of ASA Preprocedure Fasting Guidelines*

Class

Systemic Disturbance

Mortality

Ingested Material

1

Healthy patient with no disease outside of the surgical process

<0.03%

Clear liquids‡

2 hr

Breast milk

4 hr

2

Mild-to-moderate systemic disease caused by the surgical condition or by other pathologic processes

0.2%

3

Severe disease process that limits activity but  is not incapacitating

1.2%

4

Severe incapacitating disease process that is  a constant threat to life

8%

5

Moribund patient not expected to survive  24 hours with or without an operation

34%

E

Suffix to indicate an emergency surgery for any class

Increased

ASA, American Society of Anesthesiologists. From Cohen MM, Duncan PG, Tate RB: Does anesthesia contribute to operative mortality? JAMA 1988;260:2859-2863.

ASA preoperative classification can help stratify a patient’s risk for a medical event during procedural sedation/analgesia. At one author’s institution, only ASA 1 and 2 (healthy, low health risk) patients are offered procedures at the outpatient surgery center. ASA 3 and higher patients have their procedures at the main hospital with a higher medical acuity support staff. Because interventional pain procedures are almost always elective, particularly for chronic pain patients, ASA fasting guidelines should be observed as per Table 4-3. Of note, patients can have a small amount of clear liquids up to 2 hours prior to procedure. Otherwise, many surgery centers will allow the procedure to be performed only under local or topical analgesia.4 Medical morbid conditions, particularly cardiopulmonary disease, can be problematic for a nonanesthesiologist providing sedation. A history of sleep apnea and difficult airway physical habitus as specified by Table 4-4 may suggest less sedation or having a monitoring anesthesiologist for the procedure would be appropriate.

Allergies The main allergies that most interventional pain management specialists encounter are allergies to latex, iodine/contrast, or to local anesthetics.

Infant formula Nonhuman

milk§

(Light meal)

Minimum Fasting Period†

6 hr 6 hr 6 hr

*These recommendations apply to healthy patients who are undergoing elective procedures. They are not intended for women in labor. Following the Guidelines does not guarantee a complete gastric emptying has occurred. †The fasting periods apply to all ages. ‡Examples of clear liquids include water, fruit juices without pulp, carbonated beverages, clear tea, and black coffee. §Since nonhuman milk is similar to solids in gastric emptying time, the amount ingested must be considered when determining an appropriate fasting period. ASA, American Society of Anesthesiologists. (A light meal typically consists of toast and clear liquids. Meals that include fried or fatty foods or meat may prolong gastric emptying time. Both the amount and type of foods ingested must be considered when determining an appropriate fasting period.) From American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by ­non-anesthesiologists. Anesthesiology 2002;96:1004-1017.

Latex and iodine allergies can be easily prevented with advanced notice. Most interventional pain procedures can document correct placement fluoroscopically without contrast patterns and by anatomical landmarks. Surface preparation solutions, such as chlorhexidine can be used instead. Indeed, the authors routinely use chlorhexidine because some literature suggests that it may be the best antiseptic for regional and interventional pain procedures.8 Most local anesthetic allergies are caused by amide local anesthetic compounds, such as lidocaine or bupivacaine. Some patients also describe an allergy from a combination of these agents mixed with epinephrine. Often the epinephrine in a prior event was absorbed intravascularly causing an increase in heart rate. An alternative to using amide local anesthetics are esters: chloroprocaine or procaine. The main question to ask is whether the patient had a “true” allergic reaction with skin rash, throat tightness, difficulty breathing or swallowing. If the patient has a rash caused by benzocaine, a common ester local anesthetic in suntan lotions, the patient may be allergic to esters. Typically, patients are allergic to one chemical structure of local anesthetic: amides or esters; so the

Conscious Sedation for Interventional Pain Procedures  25

Table 4-4  Airway Assessment for Sedation and Analgesia Positive pressure ventilation, with or without tracheal intubation, may be necessary if respiratory compromise develops during sedation-analgesia. This may be more difficult in patients with atypical airway anatomy. In addition, some airway abnormalities may increase the likelihood of airway obstruction during spontaneous ventilation. Some factors that may be associated with difficulty in airway management are: History Previous problems with anesthesia or sedation Stridor, snoring, or sleep apnea Advanced rheumatoid arthritis Chromosomal abnormality (e.g., trisomy 21) Physical Examination Habitus Significant obesity (especially involving the neck and facial structures) Head and Neck Short neck, limited neck extension, decreased hyoid-mental distance (< 3 cm in an adult), neck mass, cervical spine disease or trauma, tracheal deviation, dysmorphic facial features (e.g., Pierre-Robin syndrome) Mouth Small opening (< 3 cm in an adult); edentulous; protruding incisors; loose or capped teeth; dental appliances; high arched palate; macroglossia; tonsillar hypertrophy; nonvisible uvula Jaw Micrognathia, retrognathia, trismus, significant malocclusion From American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by nonanesthesiologists. Anesthesiology 2002;96:1004-1017.

The provider who monitors the patient should have training and understanding of the agents that are administered and they should be readily available. Emergency equipment should be available as listed on example III from ASA guidelines.4 Most outpatient surgery centers require on-site staff with ACLS certification and/or physicians trained in anesthesiology or emergency medicine who can manage airway emergencies (Table 4-5). At the authors’ institutions, the World Health Organization (WHO) surgical guidelines are used. Just before starting a procedure, a surgical stop is initiated and documented by nursing staff. That one last check has empirically prevented allergens from being given and other procedural complications.

Nonpharmacologic Management of Procedural Pain Two main nonpharmacologic techniques have been used to reduce procedural pain: acupuncture and cognitive behavioral strategies. A recent metaanalysis review on acupuncture suggests that there is a small analgesic effect across multiple pain studies, including headache, low back pain, and postoperative pain, and it is difficult to separate whether the pain relief is independent of the psychological impact of the ritual treatment.9 The cognitive strategies of distraction and hypnosis in the treatment of procedural pain in children are clearly effective.10 It seems likely that distraction and other cognitive techniques can help with adult procedural pain as well.

Common Side-Effects and Complaints other class may be dosed during procedures. Dosing recommendations will follow later in this chapter.

Monitoring and Room Set-Up In general, a procedure room must be able to accommodate pulse oximetry, blood pressure, oxygen, intravenous access, and other monitors, a space for a designated health care provider to record the patient’s vital signs and provide medications, and enough room to place the patient on a gurney for transport. According to Medicare guidelines: ll Moderate Sedation should be provided by a qualified physician. Physician must be continuously present to monitor the patient and personally provide care. ll During Moderate Sedation, the patient’s oxygenation, ventilation, circulation, and temperature should be evaluated by whatever method is deemed most suitable by the attending physician. ll The following Centers for Medicare & Medicaid Services (CMS) requirements for Moderate Sedation should be the same as for MAC and general anesthesia with regard to the performance of presedation examination and evaluation, prescription of the sedation, care required for the completion of a record, the administration of necessary oral or parenteral medications, and the provision of indicated postoperative care. Appropriate documentation must be available to reflect preand postsedation evaluations and intraoperative monitoring. ll The Moderate Sedation service rendered must be appropriate and medically reasonable and necessary.

Adjuvants: Particularly Antiemetics Patient satisfaction is clearly an important aspect of any pain procedure. One study by Dr. Macario and others sought to survey what clinical anesthesia outcomes are important to avoid from a patient’s perspective.11 Of the patients, 24% ranked vomiting as their least desirable outcome with avoiding nausea also having high importance. The main way of avoiding nausea for interventional pain procedures is to limit the amount of opioids, such as fentanyl, for analgesia. An expert consensus was published by Dr. Gan and colleagues in 200312 for the management of postoperative nausea and vomiting. If a patient has received no prophylaxis, 5-HT3 receptor therapy is recommended, which includes ondansetron 1.0 mg, dolasetron 12.5 mg, granisetron 0.1mg, and tropisetron 0.5 mg. The panel agreed that there is no evidence of any difference in the efficacy and safety profiles of the serotonin receptor antagonists. Other alternative therapies for rescue include: droperidol 0.625 mg IV, dexamethasone 2 to 4 mg IV, and promethazine 12.5 mg IV. Of note, droperidol has a black box warning for QT prolongation and torsades de pointes as well as neuroleptic effects (Table 4-6). If a patient is known to have high risk for postoperative nausea and vomiting, dexamethasone 4 mg IV preoperatively can be highly effective both from an efficacy and cost perspective.13 One question is whether a single dose of dexamethasone IV can affect the interpretation of whether the interventional procedure has changed the patient’s pain scores. Even doses of up to 8 mg of dexamethasone preoperatively has no effect on pain and mobilization

4

26  Basic Principles of Procedures Table 4-5  Emergency Equipment for Sedation and Analgesia

Table 4-6  Antiemetic Treatment for Postoperative Nausea

Appropriate emergency equipment should be available whenever ­sedative or analgesic drugs capable of causing cardiorespiratory depression are administered. The lists below should be used as a guide, which should be modified depending on the individual practice circumstances. Items in brackets are recommended when infants or children are sedated.

Initial Therapy

Failed Prophylaxis

No prophylaxis or dexamethasone 5-HT3 antagonist* plus second agent† Triple therapy with 5-HT3 antagonist* plus two other agents† when PONV occurs <6 hr after surgery (V) Triple therapy with 5-HT3 antagonist* plus two other agents† when PONV occurs >6 hr after surgery (V)

Administer small-dose 5-HT3 antagonist* (IIA) Use drug from different class (V) Do not repeat initial therapy (IIIA) Use drug from different class (V) or propofol, 20 mg as needed in postanesthesia care unit (adults) (IIIB) Repeat 5-HT3 antagonist* and droperidol (not dexamethasone or transdermal scopolamine) Use drug from different class (V)

Intravenous equipment Gloves Tourniquets Alcohol wipes Sterile gauze pads Intravenous catheters [24-22 gauge] Intravenous tubing [pediatric “micro drip” 60 drops/mL] Intravenous fluid Assorted needles for drug aspiration, intramuscular injection ­(intraosseous bone marrow needle) Appropriately sized syringes [1-mL syringes] Tape Basic airway management equipment Source of compressed oxygen (tank with regulator or pipeline supply with flowmeter) Source of suction Suction catheters [pediatric suction catheters] Yankauer-type suction Face masks [infant/child] Self-inflating breathing bag-valve set [pediatric] Oral and nasal airways [infant/child-sized] Lubricant Advanced airway management equipment (for practitioners with ­intubation skills) Laryngeal mask airways [pediatric] Laryngoscope handles (tested) Laryngoscope blades [pediatric] Endotracheal tubes Cuffed 6.0, 7.0, 8.0 mm ID (Uncuffed 2.5, 3.0, 3.5, 4.0, 4.5, 5.0, 5.5, 6.0 mm ID) Stylet (appropriately sized for endotracheal tubes) Pharmacologic Antagonists Naloxone Flumazenil Emergency medications Epinephrine Ephedrine Vasopressin Atropine Nitroglycerin (tablets or spray) Amiodarone Lidocaine Glucose, 50% [10 or 25%] Diphenhydramine Hydrocortisone, methylprednisolone, or dexamethasone Diazepam or midazolam From American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by ­non-anesthesiologists. Anesthesiology 2002;96:1004-1017.

scores after colorectal surgery.14 Dexamethasone 8 mg can elevate postprocedural glucose concentrations in patients with impaired glucose tolerance and may not be the best first-line choice for nausea prophylaxis, especially if the patient is receiving steroids for the interventional block as well.

5-HT3 = serotonin. *Small-dose 5-HT antagonist dosing: ondansetron 1.0 mg, dolasetron 12.5 mg, granisetron 0.1 mg, and tropisetron 0.5 mg. †Alternative therapies for rescue: droperidol 0.625 mg IV, dexamethasone 2-4 mg IV, and promethazine 12.5 mg IV. From Gan TJ, Meyer T, Apfel CC, et al: Consensus guidelines for managing ­postoperative nausea and vomiting. Anesth Analg 2003;97:62-71.

Medications Sedatives and Amnestics The main goal of intravenous sedation is to provide a short duration anxiolytic and amnestic that is controlled so that airway compromise is avoided. In general, benzodiazepines are used as first line agents. Benzodiazepines induce sedation and anxiolysis by modulating GABA transmission in the CNS. GABA is one of the most common inhibitory neurotransmitters in the brain and benzodiazepines bind to GABAA receptors, increase chloride ion channel influx, and subsequently decrease neuronal excitation.15 Midazolam (Versed) is usually the most preferred benzodiazepine administered compared to lorazepam (Ativan) or diazepam (Valium) because of the shorter elimination half-life (approximately 2 hours for midazolam compared to 12 hours for lorazepam, and 20 to 50 hours for diazepam).16 Typical intermittent dosages of midazolam range from 0.5 mg to 1 mg repeated, lorazepam 0.25 mg repeated, and diazepam 1 to 2 mg repeated. Habitual alcohol usage increases the clearance of midazolam so higher dosages may be required for sedation. Lorazepam is less affected by enzyme induction and other factors that alter cytochrome P450 metabolism. Age and smoking decrease the metabolism of diazepam and can prolong sedative effects. Diazepam may be used if the patient is already taking that agent as an antispasmotic or muscle relaxant or if it is used as an anxiolytic orally many hours prior to the procedure. Midazolam is probably the preferred choice for short interventional procedures, especially if the patient is not taking chronic benzodiazepines as anxiolytics. Flumazenil is a benzodiazepine antagonist that is similar to midazolam in structure. It reverses benzodiazepine overdosage or oversedation in a dose-dependent manner. Although it is the primary benzodiazepine reversal agent available, compared with benzodiazepine antagonists (midazolam, lorazepam, diazepam), it has the highest clearance and shortest elimination half-life—approximately 1 hour.16 Hence, flumazenil will provide rapid onset of reversal but will require continued monitoring for resedation and even a

Conscious Sedation for Interventional Pain Procedures  27

continuous intravenous infusion to outlast the original benzodiazepine agonist. Flumazenil may be dosed at 0.1 to 0.2 mg every 1 to 2 minutes to a maximum of 1.0 mg. Practitioners should note that flumazenil will reverse any lowering of seizure threshold that the initial benzodiazepine dosage may have induced.

Deeper Sedation Other agents, namely etomidate, propofol, and ketamine have been utilized for procedural sedation. Etomidate and propofol can be used as induction agents for general anesthesia, so airway resuscitative measures should always be available including training by the medical provider administering the drug. Etomidate is an anesthetic induction drug that has a similar affect to benzodiazepines by increasing the number of GABA receptors and, thereby increasing GABA inhibition.15 The duration of a single dosage lasts approximately 5 minutes at standard induction dosages (0.3 mg/kg or about 20 to 40 mg) and is rapidly metabolized in the liver.17 In anesthesia, the main advantage of etomidate is that it does not produce cardiac hypotension when compared with other induction agents such as propofol. A single dose of etomidate can cause adrenocortical suppression18 as well as myoclonic activity. A single dosage of etomidate at 10 mg is used for cardioversion procedures in adults. Propofol has revolutionalized outpatient surgical procedures with its rapid onset, short duration of action, and quick recovery for patients.19 It has a chemical structure that is unrelated to other sedative hypnotic compounds18 but does affect GABA-mediated transmission. It has amnestic properties but they are not as marked as the benzodiazepines. Of note, propofol is a cardiovascular depressant and can be associated with respiratory depression at anesthetic induction doses (2 to 2.5 mg/kg or approximately 140 to 175 mg). Propofol is also extensively metabolized and excreted in the urine (>88%). There is an additive and synergistic hypnotic effect with propofol and other amnestics. So even when titrating propofol at 2.5 to 5 mg increments every few minutes after a base of midazolam and fentanyl, oversedation and respiratory compromise can occur. In addition, cognitive impairment can occur even after short procedures such as outpatient colonoscopy.20 Administration of >2 mg of midazolam was a predictor of impaired cognitive function at discharge. Typically, propofol seems to be used with interventional pain procedures that have become extended or problematic, often when moderate dosages of midazolam and/or fentanyl have been given. Ketamine is one of the oldest anesthetics (>30 years) that provides moderate sedation and analgesia in one compound. It does not suppress pharyngeal and laryngeal reflexes and can be administered in nonoperating room conditions by nonanesthesiologists.21 Ketamine produces a “dissociative” anesthetic state, which is characterized as a state of catalepsy in which the eyes remain open with a slow nystagmic gaze while corneal and light reflexes remain intact.22 The chemical structure is similar to phencyclidine (PCP) so one of the main side-effects is psychotomimetic experiences or “weird trips.”23 Ketamine’s mechanism of action is at NMDA receptors as well as cholinergic receptors of the muscarinic type and brain acetylcholinesterase. Potentiation of GABA inhibition has also been reported with high doses.24 Because of activity at NMDA receptors, ketamine could theoretically be more effective in treating neuropathic pain states or patients who are opioid tolerant.25 Current evidence

does not support routine use of ketamine for treatment of chronic pain.23 As an adjunct to outpatient interventional pain procedures, a dosage of 0.5 to 2 mg/kg (approximately 30 to 140 mg) can be administered as an induction bolus. One of the author’s recommendations would be to dose 20 to 30 mg IV bolus at one time and observe the effect, particularly if the patient has already received other sedative and analgesic agents. Ketamine undergoes extensive hepatic metabolism by the cytochrome P-450 system. It may produce hyperreactive airway reflexes, especially in the presence of inflammation of the upper respiratory tract22 and can give rise to myoclonic jerks or involuntary movements.26

Opioid Analgesics Opioid analgesic agents are the first-line medications for the relief of acute pain.27 Although morphine, the gold standard, and meperidine have been available for many years, their slower onset >10 minutes and prolonged duration of 1 to 2 hours have steered most interventional pain physicians to use the short-acting fentanyl family of synthetic opioids for procedural analgesia. All opioids act at mu receptors at the spinal cord and supraspinal levels causing a decrease in nociceptive input at the spinal lamina and activation of descending inhibitory control centers of the periaqueductal grey. Fentanyl, alfentanil, sufentanil, and remifentanil are highly lipophilic opioid analgesics compared to morphine. Fentanyl has a rapid onset of action, high clearance, and short duration of action making it ideal for procedural analgesia. Dosages of 25 to 50 mcg every 5 minutes to a total dosage of 200 mcg for healthy noncompromised patients is not uncommon for a duration of effect of 30 minutes. Fentanyl is metabolized by cytochrome P450 enzymes. The high lipid solubility leads to a slow removal in fat pools with a half-life longer than morphine; thus, the respiratory depressant effects can outlast analgesia and so postprocedural monitoring is required. Alfentanil is less lipid soluble than fentanyl and has a shorter duration of action. This agent was used to provide analgesia for the placement of peribulbar blocks in one of the author’s institutions prior to eye surgery and provided significant intraoperative analgesia but little to no postoperative analgesia. In addition, the half-life of alfentanil is shorter in children and longer in the elderly and obese, making the opioid a bit less predictable than fentanyl for standard analgesic usage. Sufentanil is approximately 10 times more potent than fentanyl and has a much higher lipophilicity. It also has a rapid onset, high clearance, and shorter duration of action than fentanyl. Dosages of 2.5 to 5 mcg every 5 minutes for a total dose of 15 mcg for a duration of effect of 15 minutes. Because of the extreme potency of this opioid, it has been often used for cardiac anesthesia or for treating extremely opioid-tolerant patients that are resistant to fentanyl. Opioid naïve patients should not be dosed with this drug without the practitioner being able to perform airway resuscitation. Remifentanil is the most lipid-soluble opioid in the fentanyl family and can provide analgesia only by continuous infusion due to ultrahigh clearance by esterases in the blood and tissues. This agent probably does not have a use in standard interventional pain procedures particularly because of the possibility of increasing postoperative pain.28 Morphine and meperidine may be used sparingly in the postoperative setting. Titrating morphine at 2 to 4 mg intravenously every 10 minutes can provide additional pain relief for

4

28  Basic Principles of Procedures

opioid-tolerant patients for a duration of 2 to 4 hours or the duration of most patient’s travel home. Nausea and urinary retention rates are higher with morphine than with fentanyl. Meperidine is a weak opioid agonist that has been used for treatment of postoperative shivers at 25 mg IV. Because higher doses (700 mg) can produce seizures from normeperidine accumulation making interpretation of local anesthetic toxicity difficult, the authors recommend not using more than 25 to 50 mg IV for perioperative shivering. The main reversal agent for all opioids is naloxone. Naloxone will reverse respiratory depression but also any opioid analgesia as well. Dosages of 40 mcg increments every 2 to 5 minutes with respiratory support can allow the patient to recover spontaneous ventilation. The duration of effect of naloxone is less than 90 minutes, which may be less than the duration of the last opioid given, usually morphine. Further naloxone dosing with continuous monitoring and respiratory support may be required.

A Brief Word on Local Anesthetics One of the main ways to decrease the dosage of drugs used for sedation and analgesia is to use an appropriate amount of local anesthetic. All local anesthetics have similar structures with an aromatic benzene ring and an amino group connected by a linkage. This linkage is either an amide or an ester. All amide local anesthetics have an “i” in their generic name before “caine”: lidocaine, bupivacaine, ropivacaine. The other local anesthetics are esters: procaine, chloroprocaine. Local anesthetics block sodium channels and stop nerve conduction of impulses. Lidocaine is typically administered in 0.5% to 2% concentrations or 5% as a topical gel. The onset of action is approximately 5 minutes with a duration of 1 to 2 hours without epinephrine. The maximal safe dose is 3 mg/kg or about 250 mg without epinephrine.

With epinephrine the safe dosage increases to 7 mg/kg or about 500 mg. Bicarbonating 0.5% lidocaine will decrease initial pain of injection site pain. Bupivacaine has a slower onset of action of 5 to 10 minutes but longer duration of action (3 to 6 hours). Typical concentrations used are 0.25% to 0.75% without epinephrine. A maximum safe dose is 150 mg without epinephrine. Bupivacaine is highly cardiotoxic so ropivacaine, a chiral version of bupivacaine is sometimes used in its place particularly for higher volume injections. Ropivacaine has concentrations from 0.2% to 1% and a maximal safe dose is 300 mg, which is less cardiotoxic than bupivacaine. One of the authors has received many calls from other physicians about patients with “lidocaine” allergies. Other than skin testing, the best option is to avoid amide local anesthetics and use an ester: chloroprocaine. 2-chloroprocaine is a rapid onset local anesthetic similar to lidocaine. It works within 5 minutes and has a duration of 30 to 60 minutes. It is the most rapidly metabolized local anesthetic in use. Prior concerns existed over reports of spinal toxicity when administered into the epidural space. New formulations have had the prior ethylenediaminetetraacetic acid (EDTA) removed, which may have caused paraspinal spasms in the past.27 Chloroprocaine may not be used if the patient reports an allergy to suntan lotion that contains benzocaine, a topical ester local anesthetic.

Postprocedural Care and Monitoring The ASA has provided thorough recommendations for recovery and discharge criteria after sedation and analgesia (Table 4-7). In general, recovery room providers must be able to assess and manage procedural complications, such as respiratory distress, seizure,

Table 4-7  Recovery and Discharge Criteria after Sedation and Analgesia Each patient-care facility in which sedation-analgesia is administered should develop recovery and discharge criteria that are suitable for its specific patients and procedures. Some of the basic principles that might be incorporated in these criteria are enumerated below. General principles 1. Medical supervision of recovery and discharge after moderate or deep sedation is the responsibility of the operating practitioner or a licensed physician. 2. The recovery area should be equipped with, or have direct access to, appropriate monitoring and resuscitation equipment. 3. Patients receiving moderate or deep sedation should be monitored until appropriate discharge criteria are satisfied. The duration and frequency of ­monitoring should be individualized depending on the level of sedation achieved, the overall condition of the patient, and the nature of the intervention for which sedation/analgesia was administered. Oxygenation should be monitored until patients are no longer at risk for respiratory depression. 4. Level of consciousness, vital signs, and oxygenation (when indicated) should be recorded at regular intervals. 5. A nurse or other individual trained to monitor patients and recognize complications should be in attendance until discharge criteria are fulfilled. 6. An individual capable of managing complications (e.g., establishing a patient airway and providing positive pressure ventilation) should be immediately available until discharge criteria are fulfilled. Guidelines for discharge 1. Patients should be alert and oriented; infants and patients whose mental status was initially abnormal should have returned to their baseline status. Practitioners and parents must be aware that pediatric patients are at risk for airway obstruction should the head fall forward while the child is secured in a car seat. 2. Vital signs should be stable and within acceptable limits. 3. Use of scoring systems may assist in documentation of fitness for discharge. 4. Sufficient time (up to 2 hr) should have elapsed after the last administration of reversal agents (naloxone, flumazenil) to ensure that patients do not become resedated after reversal effects have worn off. 5. Outpatients should be discharged in the presence of a responsible adult who will accompany them home and be able to report any postprocedure ­complications. 6. Outpatients and their escorts should be provided with written instructions regarding postprocedure diet, medications, activities, and a phone number to be called in case of emergency. From American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by  non-­anesthesiologists. Anesthesiology. 2002;96:1004-1017.

Conscious Sedation for Interventional Pain Procedures  29

neurologic events, and cognitive changes. In particular, many outpatient surgery centers are requiring physicians and other staff to have ACLS credentialing particularly if anesthesiologists or emergency medicine specialists with airway management training are not available on site. Overall, sedation and analgesia is generally a safe and rewarding experience for most patients. Preparation of the patient, physician performing the procedure, and supporting medical staff is the most important key to that success. The authors hope the information given in this chapter will help surgical or procedural centers run safely and smoothly. REFERENCES   1. Green SM, Krauss B. Procedural sedation terminology: Moving beyond “conscious sedation”. Ann Emerg Med. 2002;39:433-435.   2. Gross JB, Bailey PL, Caplan RA, et al. Practice Guidelines for sedation and analgesia by non-anesthesiologists: A report by the American Society of Anesthesiologists Task Force on Sedation and Analgesia by NonAnesthesiologists. Anesthesiology. 1996;84:459-471.   3. Smith I, Taylor E. Monitored Anesthesia Care. Int Anesthesiol Clin. 1994;32:99-112.   4. American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology. 2002;96:1004-1017.   5. Innes G, Murphy M, Nijssen-Jordan C, et al. Procedural sedation and analgesia in the emergency department. Canadian Consensus Guidelines. J Emerg Med. 1999;17:145-156.   6. Martin ML, Lennox PH. Sedation and analgesia in the interventional radiology department. J Vasc Interv Radiol. 2003;14:1119-1128.   7. Cohen MM, Duncan PG, Tate RB. Does anesthesia contribute to operative mortality? JAMA. 1988;260:2859-2863.   8. Dailey PA. Chlorhexidine or Povidone-Iodine. CSA Bulletin. 2009;58:45-47. http://www.csahq.org/pdf/bulletin/chlorhex_58_3.pdf: Accessed Nov 22, 2009.   9. Madsen MV, Gotzsche PC, Hrobjartsson A. Acupuncture treatment for pain: systematic review of randomised clinical trials with acupuncture, placebo acupuncture, and no acupuncture groups. BMJ. 2009;338:a3115. 10. Stinson J, Yamada J, Dickson A, et al. Review of systematic reviews on acute procedural pain in children in the hospital setting. Pain Res Manag. 2008;13:51-57. 11. Macario A, Weinger M, Carney S, Kim A. Which clinical anesthesia outcomes are important to avoid? The perspective of patients. Anesth Analg. 1999;89:652-658.

12. Gan TJ, Meyer T, Apfel CC, et al. Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg. 2003;97:62-71. 13. Apfel CC, Korttila K, Abdalla M, et al. A factorial trial of six interventions for the prevention of postoperative nausea and vomiting. N Engl J Med. 2004;350:2441-2451. 14. Kirdak T, Yilmazlar A, Cavun S, et al. Does single, low-dose preoperative dexamethasone improve outcomes after colorectal surgery based on an enhanced recovery protocol? Double-blind, randomized clinical trial. Am Surg. 2008;74(2):160-167. 15. Barash PG. Clinical Anesthesia. Philadelphia: Lippincott; 1993, p 388. 16. Miller’s Anesthesia. 1994:249-258. 17. Absalom A, Pledger D, Kong A. Etomidate USP Dispensing Information. Micromedex. 2001;1:1459-1461. 18. Absalom A, Pledger D, Kong A. Adrenocortical function in critically ill patients 24h after a single dose of etomidate. Anaesthesia. 1999;54(9):861-867. 19. White PF. Propofol: Its role in changing the practice of anesthesia. Anesthesiology. 2008;109:1132-1136. 20. Padmanabhan U, Leslie K, Eer AS, et al. Early cognitive impairment after sedation for colonoscopy: The effect of adding midazolam and/or fentanyl to propofol. Anesth Analg. 2009;109:1448-1455. 21. Sobel RM, Morgan BW, Murphy M. Ketamine in the ED: Medical politics versus patient care. Am J Emerg Med. 1999;17:722-725. 22. White PF, Way WL, Trevor AJ. Ketamine: Its pharmacology and therapeutic uses. Anesthesiology. 1982;56:119-136. 23. Hocking G, Cousins MJ. Ketamine in chronic pain management: An evidence-based review. Anesth Analg. 2003;97:1730-1739. 24. Raeder JC, Stenseth LB. Ketamine: A new look at an old drug. Curr Opin Anaesthesiol. 2000;13:463-468. 25. Laulin JP, Maurette P, Corcuff JB, et al. The role of ketamine in preventing fentanyl-induced hyperalgesia and subsequent acute morphine tolerance. Anesth Analg. 2002;94:1263-1269. 26. Ng KC, Ang SY. Sedation with ketamine for paediatric procedures in the emergency department—A review of 500 cases. Singapore Med J. 2002;43:300-304. 27. Raj PP. Practical Management of Pain. 3rd ed. St. Louis: Mosby; 2000: 462. 28. Guignard B, Bossard AE, Coste C, et al. Acute opioid tolerance—­ Intraoperative remifentanil increases postoperative pain and morphine requirement. Anesthesiology. 2000;93:409-417.

4

5

Radiation Safety for the ­Physician Kenneth P. Botwin, MD, Philip Ceraulo, DO, and Chunilal P. Shah, MD, MBBS, BS Currently, fluoroscopic guidance is used routinely for many interventional pain management procedures to obtain more precise localization of anatomic target areas. Fluoroscopy is used in many procedures, including swallowing studies, urologic evaluations, peripheral joint injections, and, perhaps most commonly, interventional spine procedures. The ability to perform many spinal injections, including transforaminal epidurals, facet joint injections, medial branch blocks, sympathetic blocks, discograms, and sacroiliac joint injections, is entirely dependent on fluoroscopic imaging. This chapter reviews the basic concepts of radiation safety and their practical application in the fluoroscopy suite to minimize exposure risks for the patient and spinal interventionalist.

Radiation Concepts Radiologic nomenclature describes the quantity of radiation in terms of exposure, dose, dose equivalent, and activity. Conventional terms are used in the United States, and an international system of units defined in 1960 by the General Conference of Weights and Measurements is primarily used in Europe. Each system has its unique terms (Table 5-1).1

Terminology Like matter, energy can be transformed from one form to another. When ice (solid) melts and turns to H2O (liquid) and then evaporates (gas), a transformation of matter has occurred. Similarly, x-rays transform electrical energy (electricity) into electromagnetic energy (x-rays), which then transforms into chemical energy (radiographic image). Electromagnetic energy emitted into and transferred through matter is called radiation. The spectrum of electromagnetic radiation extends more than 25 orders of magnitude and includes not only x-rays, but also the wavelengths responsible for visible light, magnetic resonance imaging (MRI), microwaves, radio, television, and cellular phone transmission (Fig. 5-1).10 Irradiation occurs when matter is exposed to radiation and absorbs all or part of it. Ionizing Radiation The two basic types of electromagnetic radiation are ionizing and nonionizing. A unique characteristic of ionizing radiation is the ability to alter the molecular structure of materials by removing bound orbital electrons from its atom to create an electrically charged positive ion. The ejected electron and the resulting positively charged atom

are called an ion pair. Ionizing radiation gradually uses its energy as it collides with the atoms of the material through which it travels. This transfer of energy and the resulting electrically charged ions can induce molecular changes and potentially lead to somatic and genetic damage. X-Rays and Gamma Rays Ionizing radiation includes x-rays and gamma rays, which are emitted from x-ray machines, nuclear reactors, and radioactive materials. Gamma rays and x-rays are identical in their physical properties and biologic effects; the only difference is that gamma rays are natural products of radioactive atoms, whereas x-rays are produced in machines. In the production of x-rays, a high dose of voltage, measured in kilovolts (kVp), and a sufficient dose of electrical current, measured in milliamperes (mA), are required. X-ray is a form of electromagnetic energy of very short wavelength (0.5 to 0.06 ångstrom), which allows it to readily penetrate matter. When an object or body is exposed to ionizing radiation, the total amount of exposure is a unit of measurement called the roentgen (R). The definition describes the electrical charge per unit mass of air (1 R = 2.58 × 10-4 coulombs/kg of air). The output of x-ray machines usually is specified in roentgen (R) or milliroentgens (mR). Ionizing radiation exposed to a body interacts with the atoms of the material it comes in contact with in the form of transfer of energy. This dose of transferred energy is called absorption, and the quantity of absorbed energy in humans is referred to as the radiation absorbed dose (rad). By definition, 1 rad = 100 ergs/g where the erg (joule) is a unit of energy and the gram is a unit of mass. The gray (Gy) is a commonly used international unit of measurement to describe absorbed dosages and can be calculated by multiplying the rad by 0.01. Biologic effects usually are related to the rad, which is the unit most often used to describe the quantity of radiation received by a patient. The rad equivalent man (rem) is the unit of occupational radiation exposure and is used to monitor personnel exposure devices such as film badges.

Radiologic Procedures Fluoroscopy In general, there are two types of x-ray procedures: radiography and fluoroscopy. Conventional fluoroscopic procedures, such as myelography, barium enemas, upper gastrointestinal series, and swallowing studies, usually are conducted on a fluoroscopic table. The conventional fluoroscope consists of an x-ray tube located 31

32  Basic Principles of Procedures

above a fixed examining table. The physician is provided with dynamic images that are portrayed on a fluoroscopic screen and the ability to hold and store (“freeze frame”) an image in memory for review or to print as a radiograph (“spot view”) for future reference. Conventional fluoroscopy is considered suboptimal for spinal interventional procedures because of the inability to manipulate the x-ray tube around the patient, and it has been virtually replaced by C-arm fluoroscopes with image intensification for use in spinal injection procedures. The C-arm permits the physician to rotate and angle the x-ray tube around the patient while the patient rests

on a radiolucent support table (Fig. 5-2). Image intensification is achieved through the addition of an image-intensifier tube located opposite the x-ray tube. The intensifier receives remnant x-ray beams that have passed through the patient and converts them into light energy, thereby increasing the brightness of the displayed image and making it easier to interpret. In the current image-intensified fluoroscopy, the x-ray tube delivers currents between 1 and 8  mA. Federal regulations limit the maximum output for C-arm fluoroscopes to 10 R/min at 12 inches from the image intensifier.

Factors Affecting Radiation Exposure Table 5-1  Radiation Quantities and Units Quantity

Conventional Unit

Exposure

SI Unit

Conversion

Roentgen (R)

Coulomb/kg of air (C/kg)

1 C/kg = 3876 R 1 R = 258 μC/kg 1 R = 2.58 × 10-4 C/kg

Dose

Rad (100 ergs/g)

Gray (Gy) (joule/kg)

1 Gy = 100 rad 0.01 Gy = 1 cGy = 1 rad 0.001 Gy = 1 mGy = 100 mrad

Dose equivalent

Rem (rad × Q)

Sievert (Sv) (Gy × Q)

1 Sv = 100 rem 0.01 Sv = 1 cSv = 1 rem 0.001 Sv = 1 mSv = 100 mrem

Activity

Curie (Ci)

Becquerel (Bq)

1 mCi = 37 MBq

Adapted from Wycoff HO: The international system of units. Radiology ­128:833-835, 1978.

Energy (eV)

X-ray imaging

Visual imaging

MR imaging

1010 109 108 107 1 MeV 106 105 104 1 nanometer 103 1 keV 102 101 100 1 micron 10−1 10−2 10−3 1 centimeter 10−4 10−5 10−6 10−7 1 megahertz 10−8 1 kilometer 10−9 10−10 10−11 1 kilohertz 10−12

Frequency (Hz) 1024 1023 1022 1021 1020 1019 1018 1017 1016 1015 1014 1013 1012 1011 1010 109 108 107 106 105 104 103 102

Exposure to ionizing radiation is an unavoidable event while performing fluoroscopic procedures. If one cannot avoid the radiation, then one must minimize its absorption by biologic tissues. The primary source of radiation to the physician during such procedures is from scatter reflected back from the patient. Of lesser concern is the small amount of radiation leakage from the equipment housing. The cardinal principles of radiation protection are: (1) maximize distance from the radiation source; (2) use shielding materials; and (3) minimize exposure time. These principles are derived from protective measures that were adopted by individuals who worked on the atomic bomb in the Manhattan Project; such measures also may be instituted in the fluoroscopic suite. In addition, the concept of ALARA (as low as reasonably achievable) should be applied in all situations of radiation exposure. Distance Distance is the most effective means of minimizing exposure to a given source of ionizing radiation. According to the inverse square law, the intensity of the radiation is inversely proportional to the square of Wavelength (m) 10−16 10−15 10−14 10−13 10−12 10−11 10−10 10−9 10−8 10−7 10−6 10−5 10−4 10−3 10−2 10−1 100 101 102 103 104 105 106

Gamma rays X-rays

Ultraviolet Visible light Infrared

Megavoltage therapy Supervoltage therapy Superficial therapy Diagnostic Contact therapy Grenz rays Violet Blue Green Yellow Red

Microwaves

Radiowaves

UHF VHF Shortwave Standard broadcast Longwave

Figure 5-1  The electromagnetic spectrum extends over more than 25 orders of magnitude. This chart shows the values of energy, frequency, and wavelength and identifies some common values and regions of the spectrum. (From Bushong S: Radiologic Science for Technologists: Physics, Biology, and Protection, 4th ed. St. Louis, Mosby, 1988, with permission.)

Radiation Safety for the Physician  33

the distance. That is, when a given amount of radiation travels twice the distance, the covered area becomes four times as large and the intensity of exposure reduces to 1⁄4 (Fig. 5-3). Therefore, at four times the distance from the source, exposure is reduced to 1⁄16 the intensity. A rough estimate of the physician’s exposure at a distance of 1 meter from the x-ray tube is 1/1000th of the patient’s exposure.6 It is therefore recommended that the technician and physician remain as far away from the examining table as practical during fluoroscopic procedures. The position of the physician’s body, especially the hands, should be closely monitored and his or her position should be kept at a maximum distance from the fluoroscope at all times.2 For example, it is advisable that the physician deliberately step away from the patient before acquiring each image and also use extension tubing during contrast injection to maximize the physician’s distance from the beam. Shielding Shielding factors include filtration, beam collimation, intensifying screens, protective apparel (e.g., leaded aprons, eyewear, and gloves), and protective barriers (e.g., leaded glass panels or drapes). Appropriate shielding of critical tissues (i.e., gonads, thyroid, lungs, breast, eyes, and bone marrow) from ionizing radiation is critical to the safe use of fluoroscopic equipment.3 In filtration, metal filters (usually aluminum) are inserted into the x-ray tube housing so that low energy x-rays emitted by the tube are absorbed before they reach the patient or medical staff. Beam collimation constricts the useful x-ray beam to the part of the body under examination, thereby sparing adjacent tissue from unnecessary exposure. It also serves to reduce scatter radiation and thus enhances imaging contrast. Protective apparel, such as a leaded apron ≥0.5 mm Pb, is mandatory to reduce exposure to the physician and technologist.3 Such shielding decreases radiation exposure by 90% to critical body areas.4 Lead-impregnated leather or vinyl aprons and gloves may be ordered in different thicknesses ranging from 0.55 mm Pb protection, which protects at 80 kVp, to 0.58 mm Pb, which protects at 120 kVp.5 The use of a leaded thyroid shield also is recommended because of the superficial location and sensitivity of the thyroid gland and to protect a limited amount of cervical bone marrow. Protective, flexible lead-lined gloves also may reduce exposure without sacrificing dexterity; however, their use is no substitute for vigilant avoidance of direct x-ray beam exposure.6 Leaded glasses or goggles will effectively eliminate approximately 90% of scatter radiation from frontal and side eye exposure. The leaded acrylic shields are made of clear lead equivalent to 0.3 mm Pb at 7-mm thickness. The lenses are leaded glass with a minimum thickness of 2.5 mm,

A

B

which creates a lead shielding with more than 97% attenuation up to 120 kVp.7 Clear, leaded glass x-ray protective barriers are available in several styles and shapes. They may be height-adjustable or full-height, floor-rolling radiation barriers or suspendable on an overhead track. They weigh between 100 and 400 lbs with lead thicknesses of 0.5 to 1.0 mm. When it is necessary to remain near the x-ray beam during a procedure, additional shielding should be used. Exposure Time To minimize exposure time to ionizing radiation, the clinician and radiologic technician need to work as a team. The technologist assists by optimally orienting the C-arm around the patient before beginning any kind of interventional procedure. The technologist also should ensure that the orientation of the C-arm is such that the x-ray tube is positioned directly under the patient to minimize scatter to that which is attenuated through the patient. The operator should minimize exposure time through the judicious use of the “beam on” controls (i.e., a foot or hand switch). If the technologist is responsible for the controls, then communication with the physician is critical to avoid unintended exposure. Training and experience of all personnel in the intricacies of complex procedures help to reduce unnecessary exposure. Fluoroscopic equipment may have features such as high- and low-dose modes, pulsed fluoroscopy,

2x Point source of X-rays

x d d

2x

x

At d (1 meter), area = x2

At 2d (2 meters), area = 4x2

Figure 5-3  When the distance from a point source of radiation is doubled, the radiation covers an area four times larger than the original area. ­However, the intensity at the new distance is only one fourth of the original ­intensity. (From Statkiewicz MA, Ritenour ER: Radiation Protection for ­Student ­Radiographers. St. Louis, Mosby, 1983, with permission.)

C

Figure 5-2  The C-arm rotated to the anteroposterior projection (A), oblique projection (B), and lateral projection (C).

5

34  Basic Principles of Procedures Low kVp, high mAs

High kVp, low mAs X-ray tube

Table 5-2  Average Annual Effective Dose Equivalent of Ionizing Radiations to a Member of the United States Population Dose Equivalenta Source

High energy, penetrating X-ray beam

Low energy X-ray beam

mSv

mrem

Effective Dose Equivalent mSv

%

Natural Radonb

24

2,400

2.0

55

Cosmic

0.27

27

0.27

8.0

Terrestrial

0.28

28

0.28

8.0

Internal

0.39

39

0.39

11

Total natural

—

—

3.0

82

X-ray diagnosis

0.39

39

0.39

11

Nuclear medicine

0.14

14

0.14

4.0

Consumer products

0.10

10

0.10

3.0

Occupational

0.009

0.9

<0.01

<0.3

Artificial Medical

A

Small absorbed dose

B

Large absorbed dose

Figure 5-4  The use of higher kilovoltage (kVp) and lower milliamperage (mAs) reduces patient dose. A, The use of high kVp and low mAs results in a highenergy, penetrating x-ray beam and a small patient (absorbed) dose. B, The use of low kVp and high mAs results in a low-energy x-ray beam, most of which is easily absorbed by the patient. (From Statkiewicz MA, ­Ritenour ER: Radiation Protection for Student Radiographers. St. Louis, Mosby, 1983, with permission.)

Other Nuclear fuel cycle

<0.01

<1.0

<0.01

<0.03

Fallout

<0.01

<1.0

<0.01

<0.03

Miscellaneousc

<0.01

<1.0

<0.01

<0.03

—

—

0.63

18

—

—

3.6

100

Total artificial Total natural and artificial

hold-and-store image capability, and beam collimation—all of which can minimize exposure time. A high kilovolt-low milliamperage approach to imaging will minimize the absorption of x-ray by the patient and improve the contrast of the visualized image (Fig. 5-4). Freeze-frame capabilities minimize repeated exposures and should be used to review the last image in preparation for needle adjustments during the procedure.

Radiation Risks to the Patient During Fluoroscopic Procedures Ionizing radiation occurs naturally in the environment: the general population usually is exposed to an individual effective dose equivalent of 360 millirem (mrem) of radioactivity per year. This exposure comes from numerous sources, the most significant of which is naturally occurring radon (Table 5-2).4,8

Assessment of Risk Risk assessment for patients subject to diagnostic and therapeutic radiographs is an inexact science, and the body of knowledge is constantly evolving. Current estimation of risk from radiographic exposure to a specific body part is based on the biologic effects of whole-body exposure (e.g., a survivor of an atomic bomb attack) converted by weight factors specific for individual organs and tissues. This concept was adopted by the International Commission on Radiological Protection in 1977 and was modified in 1991.9 Termed the effective dose equivalent, the calculation has been adopted by most authoritative bodies that determine radiation risk and recommend protective measures.

aTo

soft tissues. equivalent to bronchi from radon daughter products. The assumed weighting factor for the effective dose equivalent relative to whole-body exposure is 0.08. cDepartment of Energy facilities, smelters, transportation, etc. From National Council on Radiation Protection and Measurements (NCRP): Ionizing Radiation Exposures of the Population of the United States. Report No. 87b. Washington, DC, NCRP, 1987, with permission. bDose

Extent of Exposure Radiation exposure to the patient during fluoroscopic procedures can exceed those associated with routine radiographs. The amount of radiation absorbed by an individual patient depends on a number of unalterable factors relating to his or her habitus, including the type, density, and location of tissue involved. For example, bone absorbs more ionizing radiation than soft tissues. An obese person will absorb more radiation than a slender one. Because of the frequency of exposure, skin at the entry site is the area most susceptible to radiation-induced injury. Different tissues have varying degrees of sensitivity to ionizing radiation (Table 5-3).4,6,9 For instance, transient skin erythema can result from as little as 200 rad, and at 300 rad temporary hair loss may occur. The threshold for permanent injury is 700 rad, and doses >1800 rad can cause dermal necrosis. The skin dose is typically used to interpret a patient’s radiation exposure to diagnostic x-rays. In the absence of a dosimeter, the skin dose may be calculated using a variety of complicated techniques. In fluoroscopy, the patient’s exposure is more difficult to estimate because of the movement and variation in size of the radiation field. In the absence of absolute measurements, it usually is sufficient to estimate the fluoroscopic skin dose at 2 rad/mA/min. In order to determine the approximate exposure, first it is necessary to know the exposure time and milliamperage. For example, if a fluoroscopically guided transforaminal epidural corticosteroid injection requires

Radiation Safety for the Physician  35

5

Table 5-3  Specific Organ Cancer Risks of Radiation (Per 10,000 per Sv or Per 1,000,000 per Rem)

Table 5-4  Radiation Exposure Comparison Procedure/Activity

Exposure

Body Part

Organ or Cancer

Natural background

100-200 mrem/yr

Total body

Lumbar epidural with ­fluoroscopy—patient

2.5 rem/30 sec

Lumbar region

Lumbar epidural with ­fluoroscopy—physician

2.5 mrem*/30 sec

Total body

Swallowing ­videofluoroscopy (patient)

3 mrem/min†

Face/neck

Posteroanterior chest x-ray

10-30 mrem

Chest

CT scan of head

3-5 rem

Head

Probability of Radiation-Induced Cancer

Breast

50-200

Thyroid

50-150

Lung

50

Leukemia

15-25

Stomach

10-20

Brain

5-20

Colon

10-15

Liver

10-15

Lymphoma

4-12

Uterus

7-10

*Exposure

estimated without shielded protection and at a distance of approximately 1 meter. †Data collected by Charles Beasley, Radiation Safety Officer, St. John’s Regional Hospital, Springfield, MO, based on operation at 85 kVp/0.2 mA.

Salivary glands

5-10

Ovary

8

Bladder

4-7

Bone

2-5

Table 5-5  National Council on Radiation Protection and Measurements Recommendations for Occupational Radiation Exposure

Esophagus

2-5

1. Effective dose limits

Pancreas

2-5

Annual

50 mSv

(5 rem)

Paranasal sinuses

2-5

Cumulative

10 mSv

(1 rem) × age

From International Commission on Radiological Protection: Recommendations of the International Commission on Radiation Protection 26. Ann Int Commission Radiat Prot 1:1-53, 1977, with permission.

2. Annual dose limits for tissues and organs Lens of the eye

150 mSv

(15 rem)

Skin, hands, and feet

500 mSv

(50 rem)

Total dose equivalent

5 mSv

(0.5 rem)

Monthly dose equivalent

0.5 mSv

(0.05 rem)

3. Embryo/fetus

30 seconds to perform and the average milliamperage is 8 mA, exposure is estimated as follows: (2 rad/mA/min)(8 mA)(0.5 min) = 8 rad. The primary controllable factor contributing to patient exposure is the length of the procedure. Depending on the complexity of the procedure, exposure times can last a few moments to an hour or more. Fluoroscopes usually produce between 1 and 5 R/min of ionizing radiation. The typical rem exposure to patients during common diagnostic and treatment procedures is shown in Table 5-4. Calculating the health risks from radiation is a relatively inexact science, but the risk from low-level exposure appears small. However, this low-level exposure has a significant effect on the developing fetus.10

Radiation Risks to the Physician and Assisting Personnel The maximum safe allowable exposure limits have been established by the National Council on Radiation Protection and Measurement as a maximum permissible dose (MPD).11 The general radiation whole-body exposure guidelines allow no more than 5 rem/year (Table 5-5).

Guidelines for Exposure Several studies have evaluated radiation exposure to clinicians during fluoroscopically assisted orthopedic procedures. One study demonstrated that unprotected individuals working ≤24 inches from a fluoroscopic beam received significant amounts of radiation, whereas those working ≥36 inches from the beam received

mSv, millisievert. Adapted from National Council on Radiation Protection and Measurements (NCRP): Ionizing Radiation Exposures of the Population of the United States. Report No. 116. Washington, DC, NCRP, 1993, with permission.

an extremely low amount of radiation.12 Risk of radiation exposure to orthopedic surgeons also has been studied. One prospective study showed that radiation doses over a 6-month period were well below the maximum dose limits for ionizing radiation as recommended by the European Economic Communities (EURATOM) directives.13 Using a phantom patient, this experiment revealed that exposure to ionizing radiation during the insertion of a dynamic hip screw was minimal. Caution during fluoroscopy was recommended nevertheless. The cutaneous effects of long-term skin exposure in a physician are clearly ­visible (Fig. 5-5). Protective Measures In order to monitor the amount of radiation the technologist and physicians are exposed to, a film dosimetry system should be used to provide accurate personal dosimetry and comprehensive diagnostic evaluation. The Gardray film consists of a slim, light, clip-on badge that can easily be worn on either the torso (body badge) or extremities (finger/ring badge). The film is placed in a holder that incorporates six absorbers to optimize the determination of the type and level of exposure. Metal absorbers are U-shaped to permit the film to be filtered for radiation exposure not only from the front but also from the bottom and behind. The finger/ring badge should be worn

36  Basic Principles of Procedures

REFERENCES

Figure 5-5  Fingers of an 83-year-old general practitioner who set fractures under fluoroscopy for 35 years. Note the changes in the nails. A basal cell ­carcinoma was earlier resected from a proximal phalanx. (From Lennard TA: Fundamentals of procedural care. In: Lennard TA, ed: Physiatric Procedures in Clinical Practice. Philadelphia, Hanley & Belfus, 1995, pp 1-13, with permission.)

with the film facing the inside part of the hand nearest the radiation source. The body badge is worn in the same position closest to the radiation source each day. A badge also may be placed on protective eyewear to determine exposure to the lenses of the eye. The badges and rings are sent in monthly for processing to monitor the type and amount of radiation exposure (as measured in mrem) received by each participant. Results are reported as monthly and 12-month accumulated dosages. Exposure is divided into three dose-equivalent columns for shallow, deep, and eye lens exposures. The shallow dose equivalent applies to the external exposure of the skin or extremity and is taken as the dose equivalent at a tissue depth of 0.007 cm averaged over an area of 1 cm squared14; the deep dose equivalent applies to external whole-body exposure and is the dose equivalent at a tissue depth of 1 cm; and the eye dose equivalent applies to the external exposure of the lens of the eye and is taken as the dose equivalent at a tissue depth of 0.3 cm. Cataract development may occur with cumulative eye lens exposure of ≥400 rad.15 Clinical Application of Radiation Safety There have been several published studies that help the interventionalist to approximate their potential radiation exposure.16-21 These studies were able to predict the exact exposure based on a specific procedure. The interventionalist can therefore, based on the type of procedure, at least approximate their amount of radiation exposure.

Conclusion Through compliance with an occupational dosimetry program, the application of cautious work habits, and attention to the three essentials of radiation safety—distance, time, and shielding—the physician can minimize exposure and maximize long-term safety in the fluoroscopy suite. By using the proper safety standards, the interventionalist can thereby reduce exposure times. ACKNOWLEDGMENT The authors would like to acknowledge Carol Barragen for secretarial assistance.

  1. Wycoff HO. The international system of units (SI). Radiology. 1978;128: 833-835.   2. Boone JM, Levin DC. Radiation exposure to angiographers under ­different fluoroscopic imaging conditions. Radiology. 1991;180:861-865.   3. Marx MV: Interventional procedures: Risks to patients and personnel. In: American College of Radiology Commission on Physics and Radiation Safety: Radiation Risks: A Primer. Reston, Va. American College of Radiology; 1996: 22-25.   4. Larimore E (Radiation Consultants): [Personal communication to TA Lennard], 1994. Reported in Lennard TA: Fundamentals of procedural care. In: Lennard TA ed: Physiatric Procedures in Clinical Practice. Philadelphia, Hanley & Belfus; 1995: 1–13.   5. ProTech Radiation Apparel and Accessories, Palm Beach Gardens, FL.   6. Vehmas T. Finger doses during interventional radiology: The value of flexible protective gloves. Rofo. 1991;154:555-559.   7. ProTech Leaded Eyewear, Palm Beach Gardens, FL.   8. National Council on Radiation Protection and Measurements (NCRP): Ionizing Radiation Exposures of the Population of the United States. Report No. 93. Washington, DC, NCRP; 1987.   9. International Commission on Radiological Protection. Recommendation of the International Commission on Radiation Protection 26. Ann Int Commission Radiat Prot. 1977;1:1-53. 10. Gray JE. Safety risk of diagnosis radiology exposures. In: American ­College of Radiology Commission on Physics and Radiation Safety ed: Radiation Risks: A Primer. Reston, Va, American College of Radiology; 1996: 15–18. 11. National Council on Radiation Protection and Measurements (NCRP): Ionizing Radiation Exposures of the Population of the United States. Report No. 116. Washington, DC, NCRP, 1993. 12. Barendsen GW. Parameters of linear-quadratic radiation dose-effect relationships: Dependence on LET and mechanisms of reproductive cell death. Int J Radiat Biol. 1997;71:649-655. 13. O’Rourke PJ, Crerand S, Harrington P, et al. Risks of radiation exposure to orthopedic surgeons. J R Coll Surg Edinb. 1996;1:40-43. 14. Landauer, Inc., 2 Science Road, Glenwood, IL 60425-1586. 15. Marx MV, Niklason L, Mauger EA. Occupational radiation exposure to interventional radiologists: A prospective study. J Vasc Interv Radiol. 1992;3:597-606. 16. Harstall R, Heini PF. Mini, Orler R: Radiation exposure to the surgeon during fluoroscopically assisted percutaneous vertebroplasty: A prospective study. Spine. 2005;30(16):1893-1898. 17. Manchikanti L, Cash K, Moss T, Pampati V. Effectiveness of protective measures in reducing risk of radiation exposure in interventional pain management: a prospective evaluation. Pain Physician. 2003;6:301-305. 18. Manchikanti L, Cash K, Moss T, et al. Risk of whole body radiation exposure and protective measures in fluoroscopically guided interventional techniques: A prospective evaluation. BMC Anesthesiol. 2003;3(1):2. 19. Botwin KP, Fuoco GS, Torres FM, et al. Radiation exposure to the spinal interventionalist performing lumbar discography. Pain Physician. 2003;6:295-300. 20. Botwin KP, Freeman ED, Gruber RD, et al. Radiation exposure to the physician performing fluoroscopically guided caudal epidural steroid injections. Pain Physician. 2001;4:343-348. 21. Botwin KP, Thomas S, Gruber RD, et al. Radiation exposure of the spinal interventionalist performing fluoroscopically guided lumbar transforaminal epidural steroid injections. Arch Phys Med Rehabil. 2002;83:697-701.

Complications of Common Selective Spinal Injections: Prevention and Management

6

Robert E. Windsor, MD, FAAPMR, FAAEM, FASPM, Elmer G. Pinzon, MD, and Herman C. Gore, MD

Selective spinal injections are being performed with increasing frequency in the management of acute and chronic pain syndromes.1-3 Because these procedures require placing a needle in or around the spine, a risk of complications is always present. Therefore, knowledge about prevention of complications, and early recognition and management when they do occur, are paramount to appropriate patient care. This requires adequate physician training and appropriate patient preparation and monitoring. This chapter will discuss physician training, patient preparation and monitoring, and specific complications and their treatment (Appendix II).

Physician Training The level of physician training required to safely perform selective spinal injections is a topic of debate. This debate is fueled by differing standards from one region of the country to another, and from one specialty to another. Some people are concerned, for example, that certain physicians are performing selective spinal injections without appropriate training, thereby placing their patients at undue risk. Although it is true that uncomplicated lumbar procedures (in an otherwise healthy population) do not require the degree of training and expertise that high-risk procedures performed in a medically unstable population do, certain standards must still be met. Currently, the American Academy of Physical Medicine and Rehabilitation (AAPM&R) has adopted guidelines that recommend a minimum level of documented didactic and clinical training in complication prevention, recognition and management, spinal injection technique, and patient selection, such as that provided in an appropriate fellowship or residency program.4 This program must provide specific training in spinal injections and the recognition, prevention and treatment of related complications; and advanced cardiac life support (ACLS) certification. In addition, the residency chairman or fellowship director must be confident in the abilities of the physician in question, prior to recommending his or her approval for spinal interventions. Specifically, selective spinal injection courses alone, although valuable, do not provide enough training (or depth of training) for the novice injectionist to safely perform spinal injections in practice.

Patient Preparation Patient preparation issues include patient education,5,6 informed consent statement, NPO (nil per os; “nothing by mouth”) status, IV access, certainty that no procedural contraindications exist, patient positioning, sterile preparation and draping, supplemental intravenous (IV) fluids and oxygen, and plans for appropriate recovery following the procedure. Depending on the procedure and patient status, prophylactic antibiotics may also be included. Patient education should include a thorough description of the procedure, including potential risks, benefits, alternatives, and likely outcomes.6 An informed consent statement, confirming the conversation, should be executed. The statement should include signatures of the patient, the doctor, and a witness. Prior to the procedure, the patient should be NPO for 12 hours for solid foods and for 8 hours for fluids, preoperatively, to ensure that all gastric contents are distal to the ligament of Treitz.7 A large-bore IV (ideally 20 guage or larger) should be started in a large proximal upper-extremity or neck vein. This is to allow immediate IV access in an emergent setting. Small-gauge or peripherally-placed IV catheters do not allow adequate access to the central venous supply for resuscitative purposes when peripheral vasoconstriction occurs. Procedural contraindications or relative contraindications that may not have been present or recognized during the last physician office visit should be evaluated, such as chest pain, shortness of breath, fever, systemic infection, uncontrolled hypertension or other medical problems. If the procedure involves placement of a needle or other instrument into a disc, or implantation of a device, then preprocedure laboratory work should be performed. In addition, if the patient is recovering from a known systemic infection (e.g., pneumonia or urinary tract infection), then preprocedure laboratory work should also be performed. If the patient has coexisting medical problems (e.g., has chronic obstructive pulmonary disease [COPD], heart disease, etc.), clearance from the patient’s primary care or specialty doctor should be obtained. Depending on the patient’s problem, preprocedure laboratory work may include a complete blood count with differential diagnosis, liver function tests, urinalysis, chest radiograph, ECG, blood culture and sensitivity, urine culture and sensitivity, and erythrocyte sedimentation rate. 37

38  Basic Principles of Procedures

The patient should be positioned on the procedure table in a comfortable manner that will allow the treating physician unencumbered access to the region of the patient’s body under treatment. The patient’s position should be comfortable enough for him or her to lie still for the duration of the procedure. Care must be taken to ensure there is no region of neural compression or stretch, particularly if sedating medication will be used. Areas that are particularly vulnerable to neural compression or stretch include the ulnar nerve at the elbow and the brachial plexus.8 If necessary, use an arm board, tape, strapping or padding to make the patient more comfortable, enable him or her to hold the appropriate position, and prevent the patient’s hands from inadvertently compromising the sterile field. Sterile preparation should minimally include scrubbing the region of the body to be treated and surrounding areas with a povidone-iodine preparation and allowing it to dry. If the patient has an iodine allergy, chlorhexidine gluconate and/or isopropyl alcohol should be used. For discography or any type of implant, use a triple scrub, including isopropyl alcohol, chlorhexidine gluconate, and povidone-iodine, lasting for at least 5 minutes. Allow the povidoneiodine to dry. For these procedures, use pre- and postprocedure antibiotics, as well. The degree of sterile draping required depends on the procedure. If a lumbar epidural is being performed, draping the immediate area around the penetration with sterile towels is adequate. If a spinal implant, percutaneous discectomy, or other more invasive spinal procedure is being performed, full-body draping with a fenestrated drape, iodine-impregnated adhesive biodrapes, sterile towels, and half-sheets should be used as needed to ensure a sterile field. Supplemental fluids are important during most procedures, not just high-risk procedures. When a patient has been NPO for 3 hours (especially during morning procedures when he or she has been NPO since the night before), they are somewhat volumedepleted and more prone to vasovagal reactions. Supplemental fluids before, during, and after procedures help prevent such reactions. In addition, having fluids already flowing, in the event the patient becomes hypotensive, is advantageous; this can also help flush medication(s) through the line. Supplemental fluids should be used cautiously if the patient is volume-sensitive, such as with congestive heart failure or renal pathology. Supplemental oxygen should be dictated by the situation. If IV sedation is administered, supplemental oxygen should be used as needed to help maintain the patient’s oxygen saturation above 92%. If the patient has COPD or other pulmonary pathology, supplemental oxygen should be used sparingly because too much oxygen may further suppress respiratory drive. In addition, if the patient has chronic pulmonary disease, the treating physician must confirm that they can tolerate the position required by the procedure. If necessary, obtain clearance from the patient’s pulmonologist or internist.

Patient Monitoring Patient monitoring should minimally include blood-pressure and heart-rate monitoring. If the patient is infirm, a high-risk procedure is being performed, or IV sedation is being used, cardiac monitoring and pulse oximetry should also be employed. Baseline vital signs should be obtained before the procedure (for purposes of comparison during and after the procedure). Preprocedure hypertension should be approached with caution. A patient with cerebrovascular disease may require a

higher-than-normal blood pressure to maintain cerebral perfusion; thus, adjusting his or her blood pressure could incite a stroke. If lowering the patient’s blood pressure is medically safe and appropriate, gentle IV sedation is generally all that is required. Sublingual calcium channel blockers should be avoided. In addition, if IV sedation for the procedure is planned, blood pressure reduction with other medications should be avoided prior to sedation, as this combination of drugs could lower the blood pressure to dangerous levels. Cardiac monitoring should be employed for any patient with a significant cardiovascular history—or when known risks of the planned procedure might place the patient at risk for cardiovascular complication. In general, cardiac monitoring should be performed for any patient with a known history of myocardial infarction or angina; for any significantly invasive procedure (e.g., spinal implant); for any intraspinal cervical or thoracic procedure; for any procedure that may place a significant volume of local anesthetic or narcotic in the spinal canal or systemic circulation; or for any procedure that will require a significant amount of IV sedation. A rhythm strip should be run before, during, and after the procedure and included on the patient’s chart.

Patient Recovery The recovery of the patient following the procedure is critically important and is often ignored. The postprocedural period is when most procedure-related complications occur. Complications that can occur during the immediate postprocedure period include hypotension, vasovagal reactions, sensorimotor blockade, excessive somnolence, respiratory suppression, and cardiovascular complications arising from one or more of the aforementioned complications. For these reasons, a medically-reasonable recovery protocol (ultimately allowing the patient to recover in a monitored situation until he or she is alert, oriented, and able to tolerate fluids and ambulate as well as expected) is important. The following abbreviated version of the protocol for routine spinal-injection procedures, with minimal or no sedation, is recommended. The patient is allowed to remain in the procedure room in the recumbent position for 5 to 10 minutes under the observation of the nurse, while two additional sets of vital signs are taken. If the patient is in satisfactory condition, he or she is slowly moved to a sitting position and transferred to a wheel chair, or assisted with ambulation to the recovery area. The patient is observed there with intermittent vital-sign monitoring for at least 20 minutes, or until they have met the above criteria. Another person must drive the patient home if IV sedation was given during the procedure. If the specific intervention was more significant than a simple spinal injection (e.g., spinal implant, percutaneous discectomy), the recovery period may last up to 8 hours.. It may be necessary to hold the patient overnight if the previously listed criteria are not met. When they have met discharge criteria, they are discharged with appropriate safety and follow-up instructions.

General Complications of Spinal Injections Infectious Complications Infections, ranging from minor to severe conditions such as meningitis,9,10 epidural abscess,11-13 and osteomyelitis (Figs. 6-1 and 6-2),14,15 occur in 1% to 2% of spinal injections. Severe infections

Complications of Common Selective Spinal Injections: Prevention and Management  39

are rare and occur in from 1 in 1000 to 1 in 10,000 spinal injections. Severe infections may have far-reaching sequelae, such as sepsis, spinal-cord injury, or spreading to other sites in the body via Batson plexus or direct contiguous spreading. Poor sterile technique is the most common cause of infection. Staphylococcus aureus is the most common offending organism causing infection from skin structures. Infection from gram-negative aerobes and anaerobes may occur from inadvertent intestinal penetration. Usually, discitis from lumbar discography involves a gram-negative aerobe, is self-limited, and resolves with early recognition and administration of appropriate antibiotics. Cervical discitis, however, is often life threatening,

4

due to the aggressive gram-negative anaerobes that colonize the esophagus. If the infection is a mild cutaneous infection and the patient is immunocompetent, it will probably resolve with local disinfection. The physician should make specific hygiene recommendations and monitor this infection expectantly. If it appears to pursue a more aggressive course but does not involve spinal structures, appropriate oral antibiotics on an outpatient basis and frequent follow-up may be all that is required. If the infection appears to progress to spinal structures or spaces, or if the patient is infirm or otherwise predisposed to infection, in-patient evaluation and care with appropriate IV antibiotics is usually required. If epidural abscess occurs, emergent surgical drainage must be considered to avoid neural damage or other complications.16 Early detection and treatment of epidural or intrathecal infection is necessary to avoid morbidity and mortality. It usually manifests with severe back or neck pain, fever, and chills, with a leukocytosis developing on the third day following the injection.13 Patients with diabetes or other immunocompromised conditions are more susceptible to infection and should be followed very closely following spinal injections. With these patients, if infection is suspected or confirmed, they must be evaluated and treated aggressively. Preexisting systemic infection is a relative contraindication to spinal injection. If the spinal injection is critical to the overall care of the patient with preexisting systemic infection, the risks and benefits must be carefully weighed before performing the injection. In addition, administering prophylactic antibiotics for 72 hours before the injection should be considered. Knowing the local standards of care for preventing or treating spinal injection-related infections and routinely reviewing current microorganism susceptibilities are important.

Cardiovascular Complications

Figure 6-1  Lumbar epidural abscess (MRI view). T2-weighted image demonstrating an epidural abscess (white arrows) severely compressing the thecal sac at C-6 and C-7 levels.

Bleeding is a risk inherent to all injection and surgical procedures. The potential for bleeding during spinal injection is increased by liver disease, the consumption of warfarin or other anticoagulants,5,17,18 certain inherited anemias (such as G6PD deficiency or sickle-cell anemia), coagulopathy from any cause, and venous puncture.

Front

A

B

Figure 6-2  Vertebral osteomyelitis and paraspinal abscess (CT scan view). A, Note the paraspinal soft tissue mass in front of the destructive process of the L-5 vertebra. B, Soft tissue windows following intravenous contrast enhancement showing the large multilocular abscess in the soft tissues enhanced (black arrows).

6

40  Basic Principles of Procedures

The epidural vasculature is injured in 0.5% to 1% of spinal injections on average, and is more common with placement of the needle in the lateral portion of the spinal canal than the midline.19 Significant epidural bleeding may cause the development of an epidural hematoma. Clinically-significant epidural hematomas are rare, with a reported incidence of less than 1 in 4000 to 1 in 10,000 lumbar epidural cortisone injections; and may lead to irreversible neurologic compromise if not surgically decompressed within 24 hours.19-25 Retroperitoneal hematomas may occur following spinal injection if the large vessels are inadvertently penetrated. These hematomas are usually self-limited but may be a cause of acute hypovolemia or anemia. In addition to bleeding, a variety of dysrhythmias may occur. When a dysrhythmia occurs, treatment should be initiated immediately. The entire team of primary care physicians (PCPs) must be able to function synergistically when treating a dysrhythmia. ACLS code scenarios should be run in the procedure facility no less than quarterly; all PCPs should know how to alert other staff and extended PCPs immediately; and everyone should know their specific roles in such situations. In addition, all PCPs should know where emergency care equipment is located and how to use it within the limits of their roles. Treatment of individual dysrhythmias is beyond the scope of this chapter; however, the reader is directed to the Emergency Cardiac Care Algorithms included in Appendix I and other sources for more detailed information.26,27

Neurologic Complications Neurologic complications are rare. The most common causes of neural injury during spinal injection are: direct trauma to the spinal cord or nerve roots from a needle; compression from an epidural hematoma; or involvement by infectious exudate. Other causes include stroke from injection-, sedation- or cardiac-induced hypotension; dislodgement of plaque from intraarterial injection; or anoxia from respiratory arrest or laryngeal obstruction. The proximity of the vertebral artery during cervical transforaminal or facet joint injections requires particular knowledge of the three-dimensional anatomy of the cervical spine, as well as specific training and expertise in cervical spinal-injection procedures, to consistently protect these structures. Injection into this vessel may cause a posterior circulation stroke, hematoma formation and occlusion of the vessel, or injection of air. Seizure may also occur if local anesthetic is injected into the vessel. Studies demonstrate that fluoroscopically-guided spinal injections are less apt to cause inadvertent neural injury or injection into a vascular structure.28 A pertinent neurologic review of symptoms and a physical examination should be performed immediately if a neurologic complication is suspected.

Respiratory Complications Respiratory arrest occurs when a patient becomes apneic for greater than 1 minute, due to lack of central respiratory drive or paralysis of the muscles of respiration.29 Respiratory arrest may occur from a variety of causes, including oversedation, central nervous system trauma, and intrathecal or epidural injection of a sufficient amount of local anesthetic to cause spinal anesthesia. Treatment requires immediate recognition of the condition and emergent support of vital signs. If the cause is self-limited, treatment may require the support of respiration and other vital signs as needed until spontaneous and adequate respiration

resumes. If the cause can be easily reversed, it should be (as when too much narcotic or sedative has been given). In this particular situation, it is important to remember the half-life of the reversing agent, compared to the half-life of the narcotic or sedative being reversed. If the narcotic or sedative’s half-life is longer than that of the reversing agent, respiratory compromise may resume when the reversing agent has been metabolized. The true incidence of respiratory depression due to spinal opioid administration is unknown. Factors that may cause respiratory depression include the use of sedatives, parenteral or spinal opioids, and local anesthetics. One of the main advantages of spinal versus parenteral opioid administration is the lack of respiratory depression with the former.30 It should be emphasized that respiratory rate alone is inadequate to establish the presence or lack of respiratory depression. The measurement of blood gases remains the preferred option.29 Other respiratory complications due to spinal injections include pneumothorax and injury to the recurrent laryngeal nerve. A pneumothorax may occur during a lower cervical procedure such as a discogram, selective nerve root block, or thoracic procedure (such as an intercostal nerve block). As a general rule, a pneumothorax may not occur if a needle penetrates the pleural cavity or lung parenchyma, unless it is placed through a bleb, the needle is 18-gauge or larger, or a solution has been injected. When a pneumothorax does occur, it is usually self-limited and causes only minor collapse(s) of the lung (10%).31 Treatment includes close observation with supportive care, usually in a hospital, and serial chest radiographs. A chest tube should be placed if the pneumothorax advances significantly over 25% or the patient develops shortness of breath or other signs of respiratory distress. Injury to the recurrent laryngeal nerve may cause unilateral vocal-cord paralysis, reduced ability to protect the airway, and hoarseness. This injury is usually self-limited and resolves on its own; but it may be clinically significant while the patient is recovering from sedation, or when there is preexisting underlying pathology that causes marginal airway protection (e.g., stroke or laryngeal cancer).

Urological Complications The application of local anesthetics and/or opioids to the lumbar and sacral nerve roots results in higher incidence of urinary retention.32 This side-effect of lumbar epidural nerve block is seen more commonly in elderly males, multiparous females, and patients who have undergone inguinal and perineal surgery. Overflow incontinence may occur if such a patient is unable to void or bladder catheterization is not utilized. All patients undergoing lumbar epidural nerve block should demonstrate the ability to void the bladder prior to discharge from the pain center.

Dural Puncture In the hands of the experienced interventional spine specialist, inadvertent dural puncture during lumbar epidural injections should occur in <0.5% of cases (or 1 in 200 epidural injections).33 This occurs when the dura mater is violated by the epidural needle, and a sufficient amount of cerebrospinal fluid leaks out from the thecal sac, causing a positional headache.34-37 The rare occurrence of postdural puncture (spinal-tap) headache is an annoying side effect, but is generally benign for the most part and will pass without permanent harm or morbidity to the patient.

Complications of Common Selective Spinal Injections: Prevention and Management  41

Rarely, with dehydration and severe nausea and vomiting, uncal herniation may occur, with associated brainstem involvement and potentially death.38 If a needle is placed subdurally and epidural doses of local anesthetics are administered, the signs and symptoms are similar to subarachnoid injection.39 The subdural or subarachnoid injection of large doses of local anesthetics may cause total spinal anesthesia, loss of consciousness, hypotension, cardiovascular arrest, apnea, and even death. This condition requires immediate resuscitative measures and support of all vital signs until the condition resolves. Intubation is usually required to adequately control the airway and ventilate the patient.

Fluoroscopic Exposure Epidural injections performed without fluoroscopy are not always placed into the epidural space, at the desired vertebral interspace; or the medication does not get to the desired target organ due to anatomic abnormality, as noted in various sources.40-48 For this reason, most spine-management specialists recommend fluoroscopic direction and the use of nonionic or low ionic contrast agents for epidural injections. This helps confirm accurate needle placement and the delivery of the injected solution to the appropriate target organ.48 The risk of fluoroscopic exposure to the patient is minimal, for one procedure or several isolated ones because each procedure should require minimal (<20 seconds) fluoroscopic exposure time. Related exposure to the physician, attending nurse, x-ray technician, and anyone else consistently in the procedure room should be viewed as cumulative. To limit exposure to these patient care providers (PCPs), it is important to note that radiation dissipates at the inverse of the square of the distance from the tube. As a result, if PCPs are able to stand six feet or more away from the fluoroscopic tube, their risk of excessive exposure is minimal. The fluoroscopy anode should also be kept under the procedure table because this anode is the source of the radiation. With these precautions, the patient absorbs the bulk of the directed radiation. The vast majority of the relatively small amount of other radiation spilled into the room is known as “scatter radiation”, which has much less ability to penetrate tissues than directed radiation. In addition, the PCPs should wear appropriate protective garments. The physician should wear a lead apron, thyroid shield, radiation-attenuating gloves, and perhaps lead-lined glasses. The nurse and x-ray technician should wear wrap-around lead aprons because their backs are frequently turned toward the radiation source, and thyroid shields. All PCPs should wear radiation badges on their thyroid shields and aprons; and the physician should consider wearing a ring badge, if his or her hand is routinely in the radiation field during active fluoroscopy. Finally, the fluoroscopy unit must be routinely maintained and inspected to confirm its proper function and safety. Proper fluoroscopy use (including safe radiation practices) can direct and confirm accurate needle placement, maximizing benefits while limiting potential risks for patients and PCPs.

Medication Reactions Adverse drug reactions are rarely seen with medications used during spinal injections. The treating physician should be aware of drug toxicity, side effects, allergic reactions, and concentration and dosing of all medicines used.

Lidocaine and bupivacaine are the most common local anesthetics used during spinal injections. Awareness of their potential central nervous system (CNS) effects, cardiovascular toxicity, and side effects is very important. Strict cardiovascular and neurologic monitoring is required before, during, and after the procedure. Although most anaphylactic reactions typically occur within 2 hours after the epidural injection, they have been known to occur up to 6 hours later.49 Local anesthetics primarily function by reversibly blocking sodium channels in nerve and muscle membranes, having a direct effect on sympathetic nerves when injected into the subarachnoid space and the cardiac tissue (when injected intravascularly). If the sympathetic system is sufficiently blocked, hypotension may result; and if cardiac muscle is sufficiently blocked, decreased contractility may result. When injected intravenously, lidocaine is “fast-in and fast-out,” reaching steady state in one to two heart beats. Bupivacaine is “fast-in and slow-out,” and its blocking action increases as the heart works harder. These are the main direct effects that can cause cardiac arrest. Cervical and thoracic level blocks have an increased risk for complications because of the regional neural supply to the heart and respiratory control. Central nervous-system toxicity by 1% lidocaine has an onset at plasma concentrations of 5-10 mcg/mL, which is slightly more than 400 mg (or 40 mL) of total intravenous bolus. Bupivacaine is about four times more toxic than lidocaine, with a toxic bolus of 100 mg (or 10 mL).50 A person with CNS toxicity usually presents with complaints of circumoral numbness, disorientation, lightheadedness, nystagmus, tinnitus, and/or muscle twitching in the face or distal extremities. Peak plasma concentrations occur 10 to 20 minutes after injection. For that reason, patient monitoring for at least 30 minutes following an epidural injection with a significant bolus of lidocaine or bupivacaine is mandatory. Methylprednisolone, triamcinolone, and betamethasone are the most commonly used corticosteroid preparations. Side effects are uncommon but could include headache, dizziness, insomnia, facial erythema, rash and pruritus, low-grade “fever” (<100° F), hyperglycemia, transient hypotension and hypertension, increased back or limb pain, fluid retention, mood swing, euphoria, menstrual irregularity, and gastritis.17 Other rare side effects include elevation of cerebrospinal-fluid protein levels, septic or aseptic meningitis, worsening of multiple sclerosis symptoms, sclerosing spinal pachymeningitis, exacerbation of latent infection, near-fatal septic meningitis (intrathecal injection), hypercorticism, and congestive heart failure. Anaphylactic and Allergy Reactions Anaphylactoid (without histologic immune response) and anaphylaxis (with a histologic immune response) occur most often within 2 hours after the epidural injection, and have been known to develop up to 6 hours later.49 These usually cause fatalities by respiratory-related complications involving mechanical airway obstruction. Therefore, monitoring patients closely for approximately 30 minutes after the procedure is recommended. Informing the patient about possible risks and side effects can also expedite early identification of complications. Bleeding Complications Epidural hematoma formation following injection is extremely rare. Bleeding usually occurs because of damage to the veins in the highly vascular epidural space. Medications that interfere with the clotting

6

42  Basic Principles of Procedures

mechanism include heparin, warfarin, aspirin, and most nonster­ oidal anti-inflammatory drugs (NSAIDs).5,17,18 Patients usually present with severe neck or back pain, associated with any significant neurologic complaint, right after the procedure.17 An immediate physical examination, followed by a computer tomography (CT) scan or MRI (magnetic resonance imaging) scan, is essential for patients thought to have an epidural hematoma because early surgical intervention can limit or even prevent permanent neurologic damage (Fig. 6-3).

Specific Complications of Selective Spinal Injections Lumbar Epidural Injections The lumbar epidural space is highly vascular. Inadvertent intravenous placement of the epidural needle occurs in approximately 0.5% to 1% of patients undergoing lumbar epidural anesthesia.33 This rare complication is mostly seen with distended epidural veins, such as those present in pregnant patients and patients with large abdominal tumor masses. If the misplacement is unrecognized, injection of a large volume of local anesthetic directly into an epidural vein may result in significant local anesthetic toxicity.51 Careful four-quadrant aspiration (aspiration in all four quadrants by rotating the needle), prior to injection of drugs into the epidural space, is mandatory in identifying the vascular placement of the needle when performing a “blind” (nonfluoroscopically-guided) epidural injection. Neurologic complications of lumbar nerve block are uncommon if proper technique is used. Usually, these complications are associated with a preexisting neurologic lesion or with surgical or obstetric trauma, rather than with the lumbar block itself.32 Direct trauma to the spinal cord or nerve roots is usually accompanied by pain. Any significant pain that occurs during placement of the epidural needle or catheter, or during injection, should warn the injectionist to pause and confirm needle placement before proceeding.33 The use of deep intravenous sedation or general anesthesia prior to initiation of epidural nerve block may reduce the patient’s ability to provide accurate verbal feedback if needle misplacement occurs. Therefore, conscious sedation or general anesthesia prior to epidural nerve block should be employed with caution.52 When the patient’s lower-extremity neurologic status deteriorates rapidly or when a cauda equina syndrome is suspected within 24 to 48 hours following an epidural procedure, an expanding epidural hematoma should be considered.53 If the injectionist suspects that diagnosis, an immediate and complete clinical evaluation is mandatory. If the diagnosis is still suspected following the clinical evaluation, a lumbar CT scan or MRI scan should be obtained (Figs. 6-4 through 6-6). If the diagnosis is confirmed, an emergent surgical consult to consider decompression should be arranged.

Caudal Epidural Injections Incorrect needle placement during caudal epidural injection occurs 25% to 40% of the time.54,55 The needle may be placed outside the sacral canal, resulting in injection of air or fluid into the subcutaneous tissues, periosteum, sacrococcygeal ligament, sacral marrow cavity, and/or pelvic cavity, possibly entering both the rectum and/ or vaginal vault.

Figure 6-3  Acute epidural hematoma and subarachnoid hemorrhage (CT scan view). Thoracic spine view showing a lenticular, high-density epidural hematoma (open arrow) causing spinal cord compression. Acute hemorrhage is noted in the subarachnoid space.

The application of local anesthetic and opioids to the sacral nerve roots results in increased incidence of urinary retention, especially in elderly males and multiparous females, and after inguinal and perineal surgery. The use of smaller doses of local anesthetic will help avoid these burdensome complications, without adversely affecting the efficacy of caudal epidural steroid injections when treating painful conditions.56 Because of the proximity of the sacral hiatus to the perineum, there is increased incidence of epidural abscess and meningitis compared to the interlaminar or transforaminal injection route. When placing the epidural needle, remembering that the thecal sac usually ends at the S2 bony level, but may end as low as S4, is important. Therefore, the needle should be placed no higher than absolutely necessary to assure epidural injection. If the needle penetrates the thecal sac, results may include a positional headache and/or lowering of the body’s protection against meningitis because the thecal sac will have been violated. In addition, if this needle malposition is not detected prior to injection, an intrathecal injection may occur—potentially causing a spinal block and its associated sequelae.

Cervical Epidural Injections Because of the potential for hematogenous spread via Batson plexus, local infection and sepsis represent absolute contraindications to the cervical approach to the epidural space. Anticoagulation and coagulopathy also represent absolute contraindications to cervical epidural nerve block because of the risk of epidural hematoma.5,6,17,18 Because the spinal cord lies within the spinal canal, there is increased risk for spinal cord injury with the injection technique, as compared to lower- or midlumbar injections. Central canal stenosis, either from bony eburnation, central disc herniation, or congenital shortening of the pedicles, represents an absolute contraindication to performing an interlaminar epidural injection at that level (Figs. 6-7 and 6-8).57,58

Complications of Common Selective Spinal Injections: Prevention and Management  43

6

A

B

Figure 6-4  Herniated nucleus pulposus (MRI view). A, T1-weighted sagittal image showing impingement of the thecal sac by the herniated nuclear material (white arrow). B, Axial sagittal gradient echo image showing the herniation shifted to the left (black arrow).

Figure 6-5  Posterolateral disc herniation (CT scan view). Left-sided focal protrusion of the disc (black arrow), leading to posterior displacement of the left S1 nerve root (open arrow) and effacement of the anterior epidural fat. This is in contrast to the epidural fat on the right and normal location of the right S1 nerve root (white arrow).

Thoracic Epidural Injections Thoracic epidural techniques are similar to lumbar techniques; but the presence of the narrow epidural space, and proximity to the spinal cord in the thoracic vertebral canal, makes spinal cord trauma more likely. The incidence of spinal cord damage is unknown, although the incidence of infection is increased in the thoracic spine when compared to the lumbar spine.59 The presence of the lungs on either side of the spine makes a pneumothorax a potential complication not usually considered with either a cervical or lumbar injection. The injection of local

Figure 6-6  Posterolateral disc herniation (lumbar myelogram view). Oblique view performed with water-soluble contrast revealing the abrupt termination and widening of the S1 nerve root sleeve (white arrow).

anesthetic in the mid-thoracic epidural space may cause inhibition of the cardiac accelerator zone, causing hypotension and bradycardia and its potential sequelae. In addition, a thoracic motor block from either the epidural or intrathecal injection of local anesthetic can cause up to 50% reduction in tidal volume, making adequate ventilation of a patient with pulmonary disease difficult.

44  Basic Principles of Procedures

Figure 6-7  Degenerative central spinal stenosis (schematic view). Lumbar vertebra at the disc level is noted in the axial view. It is noted that the osteophytes derived from the articular processes can lead to thecal sac compression.

Selective Nerve Root Blocks Selective nerve root blockade has been used interchangeably as a spinal nerve block, selective epidural, or an anterior ramus block.48 In this brief discussion we will deal with each separately. A spinal nerve block occurs when the needle tip is placed within the neural foramen; and local anesthetic affects only the spinal nerve and does not migrate inside the spinal canal. The main risk of this injection technique is trauma to the spinal nerve or dorsal root ganglion. If the needle penetrates the dural sleeve, an intrathecal injection may occur with associated risks and complications. A selective epidural occurs when fluid is injected into the epidural space via a neural foramen. To accomplish this, the needle is also placed within the neural foramen; thus, trauma to the spinal nerve or dorsal root ganglion is possible. Injection into the dural sleeve is also possible—with all its associated risks and complications. An anterior ramus block is an extraspinal injection of the anterior ramus. This occurs 1 to 2 cm outside of the neural foramen and local anesthetic does not reach the spinal canal or spinal nerve. The main complication of this blockade is direct trauma to the anterior ramus from the needle or the disruption of the neural vasculature, causing an intraparenchymal hematoma or neural infarct.

Discography The most common severe complication after discography is infection of the disc, commonly referred to as discitis. This should occur no more frequently than in 1 in 500 to 1 in 750 discs injected.60,61 The most common organisms infecting the lumbar disc are S. aureus and Staphylococcus epidermidis.60,62 Occasionally, a colonic organism involves the lumbar discs, resulting from penetration of the colon with the discography needle. Because of the limited blood supply of the disc, such infections may prove difficult to eradicate. Discitis usually manifests as an increase in spine pain 5 to 14 days following discography. Acutely, there should be no change

Figure 6-8  Central spinal stenosis (CT scan view). Marked hypertrophy of the ligamentum flavum (open arrows) is noted to directly cause thecal sac compression; also seen is mild annular bulging and facet joint arthropathy.

in the patient’s neurologic status. An elevated sedimentation rate will be seen within the first week to 10 days.63-65 The preferred option in the detection of discitis is now considered to be magnetic resonance imaging (MRI), which was found to be superior to bone scanning with a 92% sensitivity, 97% specificity, and 95% overall accuracy (Fig. 6-9).66-68 The incidence of thoracic discitis following a thoracic discogram is unknown, but the organisms infecting those discs following discography should be similar to those involving the lumbar discs. Similarly, the incidence of pneumothorax and large-vessel damage following thoracic discography is also unknown. In one series of 230 outpatient thoracic discograms, Schellhas reported a zero incidence of pneumothorax.69 Although this is encouraging, the complication does still occur; thus, the procedure should not be attempted without substantial experience and training. Cervical discitis is generally profound and life threatening. The esophagus has gram-negative and anaerobic bacteria as components of its normal flora. Therefore, placing the discography needle through it and into the disc may seed the disc with bacteria that may initiate a profound infection. In the mid- and lower-cervical spine, the esophagus lies on the left side of the larynx. The carotid sheath lies on the anterolateral surface of the cervical spinal column. As a result, a cervical discogram should be performed using a right-sided paralaryngeal approach. In performing this approach, the esophagus should be pushed to the left and the carotid sheath to the right, thereby minimizing the risk of trauma to these structures. If the needle does penetrate the carotid sheath, direct injury to the vagus nerve or carotid artery could occur with associated risks and complications. In addition to infectious complications, pneumothorax may occur after cervical and thoracic discography. This complication should rarely occur if appropriate techniques are used. Most pneumothoraces following cervical or thoracic discography are small (10% to 15% of lung volume) and can often be treated conservatively. However, all pneumothoraces must be taken seriously and observed overnight, with serial chest radiographs and close

Complications of Common Selective Spinal Injections: Prevention and Management  45

3

technique requires deeper penetration of the needle into the joint and toward the spinal structures. Local anesthetic may leak out of the joint into these areas, causing motor and sensory blockade with attendant risks and complications. Third occipital nerve blocks can cause transient ataxia and unsteadiness due to partial blockade of the upper cervical proprioceptive afferents and the righting response.76,77 In one study of cervical facet joint radiofrequency denervation, 13% of patients complained of postprocedure pain that resolved in 2 to 6 weeks. Four percent of patients complained of occipital hypesthesia, probably due to a lesion of the third occipital nerve, which resolved in 3 months.77 No persistent motor or sensory deficits occurred.

Sympathetic Nerve Blocks

Figure 6-9  Lumbar disc space infection (MRI view). T1-weighted image showing areas of low signal of the L-4 and L-5, with the anterior paraspinal mass noted (white arrow).

monitoring of vital signs and blood gases. If the pneumothorax progresses, a chest tube must be placed. Direct trauma to the nerve roots and the spinal cord can occur if the needle is allowed to traverse the entire disc or is placed too laterally. These complications should rarely occur if appropriate techniques and precautions are used. Such needle-induced trauma to the cervical spinal cord can result in syrinx formation with attendant progressive neurologic deficit, including quadriplegia.

Intercostal Nerve Blocks Given the proximity of the pleural space, pneumothorax after intercostal nerve blocks is a distinct possibility. The incidence of the complication is less than 1% (0.082%),70 but it occurs with greater frequency in patients with chronic obstructive pulmonary disease. Because of the proximity to the intercostal nerve and artery, when analgesia is produced from the intercostal block, the compensatory vasoconstriction eases, and the patient may become hypotensive. In a similar manner, intercostal blocks can lead to respiratory failure when pain relief from the block unmasks the ventilatory depression of previously administered, but ineffective, parenteral narcotics.71

Facet Joint Nerve Blocks The problem cited most often with these procedures is a transient exacerbation in pain (about 2% incidence), lasting as long as 6 weeks to 8 months in some cases.17,72,73 Spinal anesthesia may occur after facet joint injection if the needle is positioned within the thecal sac, or if there is an abnormal communication between the facet joint capsule and the thecal sac. Chemical meningitis after lumbar facet block has been reported.73-75 These complications are thought to have occurred after inadvertent dural puncture. Facet-capsule rupture also occurs, especially if more than 2.0 mL of injectate is used for intraarticular injections.48 During performance of cervical facet blockade, there is potential risk of entry into the intervertebral foramen, spinal canal, and vertebral artery. These complications occur more frequently using a lateral intraarticular technique than with blockade of the medial branches innervating the cervical facets because the former

In the cervicothoracic (stellate ganglion) block, acute, potentially lifethreatening complications may occur, including seizure, spinal block, hypotension, or pneumothorax.78-82 Additional complications could include block or injury to the recurrent laryngeal nerve, phrenic nerve, sympathetic trunk, apex of the lung, or brachial plexus. In the lumbar sympathetic block, potential complications include intravascular injections, intradural injections with spinal anesthesia or postural headaches, hypotension, lumbar-plexus block, renal puncture, or genitofemoral neuralgia.79,83,84 Other risks include injury to the spleen, intestines, and/or liver, and injection of large volumes of local anesthetic into the aorta or inferior vena cava. REFERENCES   1. Falco FJ. Lumbar spine injection procedures in the management of low back pain. Occup Med. 1998;13(1):121-149.   2. Moskovich R. Epidural injections for the treatment of low back pain. Bull Hosp Jt Dis. 1996;55(4):178-184.   3. Kinard RE. Diagnostic spinal injection procedures. Neurosurg Clin N Am. 1996; 7(1):151-165.   4. PASSOR: PASSOR Fellowship Guidelines. Endorsed by the AAPM&R Board of Governors; 1998.   5. PASSOR: PASSOR Educational Guidelines for Interventional Spinal Procedures. Accepted by the PASSOR Board of Governors and AAPM&R Board of Governors; June, 2001; Update, 2004.   6. North American Spine Society. Epidural Steroid Injections. General Information. 2008-2009.   7. Demling R. Preoperative Care. In: Way LW, ed. Current Surgical Diagnosis and Treatment. Conn. Appleton & Lange: Norwalk; 1991, p.9.8.   8. Sunderland S. Nerves and Nerve Injuries. 2nd ed. Edinburgh: Churchill Livingstone; 1978.   9. Dougherty Jr JH, Fraser RA. Complications following intraspinal injections of steroids: Reports of two cases. J Neurosurg. 1978;48:1023-1025. 10. Gutknecht DR. Chemical meningitis following injections of epidural steroids. Am J Med. 1987;82(3):570: [Letter]. 11. Shealy CN. Dangers of spinal injections without proper diagnosis. JAMA. 1966;197:1104-1106. 12. Goucke CR, Graziotti P. Extradural abscess following local anesthetic and steroid injection for chronic low back pain. Br J Anaesth. 1990;65(3):427-429. 13. Chan ST, Leung S. Spinal epidural abscess following steroid injection for sciatica. Case report. Spine. 1984;14(1):106-108. 14. Tham EJ, Stoodley MA, Macintyre PE, Jones NR. Back pain following postoperative epidural analgesia: An indicator of possible infection. Anaesth Intensive Care. 1997;25(3):297-301. 15. Cooper AB, Sharpe MD, et al. Bacterial meningitis and cauda equina syndrome after epidural steroid injections. Can J Anaesth. 1996; 43(5 Part 1):471-474. 16. Baker AS, Ojemann RG, Swartz MN, Richardson Jr EP. Spinal epidural abscess. N Engl J Med. 1975;293:463-468.

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46  Basic Principles of Procedures 17. University of Rochester Spine Center; Department of Orthopaedic ­Surgery; Department of Physical Medicine & Rehabilitation; University of Rochester School of Medicine; Strong Memorial Health System: What Are Possible Side Effects and Complications of Spine Procedures? 2007. 18. Derby R, Baker RM, Lee CH, Anderson PA. Evidence-informed management of chronic low back pain with intradiscal electrothermal therapy. Spine J. 2008;8:80-95. 19. Bonica JJ. Diagnostic and therapeutic blocks. A reappraisal based on 15 years’ experience. Anesth Analg. 1958;37:58-68. 20. Odoom JA, Sih IL. Epidural analgesia and anticoagulant therapy: Experience with one thousand cases of continuous epidurals. Anesthesia. 1983;38:254-259. 21. Rao TL, El-Etr AA. Anticoagulation following placement of epidural and subarachnoid catheters: an evaluation of neurologic sequelae. Anesthesiology. 1981;55:618-620. 22. Delaney TJ, Rowlingson JC, Carron H, et al. Epidural steroid effects on nerves and meninges. Anesth Analg. 1980;59:610-614. 23. Knight CL, Burnell JC. Systemic side-effects of extradural steroids. ­Anaesthesia. 1980;35:593-594. 24. Goebert Jr HW, Jallo SJ, Gardner WJ, Wasmuth CE. Painful radiculop­ athy treated with epidural injections of procaine and hydrocortisone acetate: results in 113 patients. Anesth Analg. 1961;40:130-134. 25. Knutsen O, Ygge H. Prolonged extradural anesthesia with bupivicaine at lumbago and sciatica. Acta Orthop Scand. 1971;42:338-352. 26. American Heart Association. Textbook of Advanced Cardiac Life Support. 3rd ed. 1993. 27. American Heart Association. Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiac Care. JAMA. 1992;268(16):2171-2302. 28. Racz G. Personal communication. Lubbock, Texas. 29. Rawal N, Wattwil M. Respiratory depression following epidural morphine: An experimental and clinical study. Anesth Analg. 1984;63:8-14. 30. Rawal N, Arntr S, Gustafsson LL, Allvin R. Present state of epidural and intrathecal opiate analgesia in Sweden. A nationwide follow-up survey. Br J Anaesth. 1987;59:791-799. 31. Bridenbaugh PO, DuPen SL, Moore DC, et al. Post-operative intercostal nerve block analgesia versus narcotic analgesia. Anesth Analg. 1973;52:81-85. 32. Armitage EN. Lumbar and thoracic epidural. In: Wildsmith JAW, Armitage EN, eds. Principles and Practice of Regional Anesthesia. New York: Churchill Livingstone; 1987:109. 33. Bromage PR. Complications and contraindications. In: Bromage PR, ed. Epidural Analgesia. Philadelphia: WB Saunders; 1978:654-711. 34. Benzon H. Epidural steroid injections for low back pain and lumbosacral radiculopathy. Pain. 1986;24:277-295. 35. Swerdlow M, Sayle-Creer W. A study of extradural medication in the relief of the lumbosciatic syndrome. Anaesthesia. 1970;25:341-345. 36. Warr A, Wilkinson JA, Burn JM, et al. Chronic lumbosciatic syndrome treated by epidural injection and manipulation. Practitioner. 1972;209:53-59. 37. Kepes ER, Duncalf D. Treatment of backache with spinal injections of local anesthetics, spinal and systemic steroids: A review. Pain. 1985;22(1):33-47. 38. Deisenhammer E. Clinical and experimental studies on headaches after myelography. Neuroradiology. 1975;9:99-102. 39. Waldman SD. Subdural injection as a cause of unexplained neurological symptoms. Reg Anesth. 1992;17:55. 40. El-Khoury Ehara S, Weinstein JN, et al. Epidural injections: A procedure ideally performed with fluoroscopic control. Radiology. 1988;168: 554-557. 41. Mehta M, Salmon N. Extradural block. Confirmation of the injection site by x-ray monitoring. Anaesthesia. 1985;40:1009-1012. 42. Dreyfuss P. Epidural steroid injections: A procedure ideally performed with fluoroscopic control and contrast media. ISIS Newsletter. 1993;1(5). 43. Stewart HD, Quinnell RC, Dann N. Epidurography in the management of sciatica. Br J Rheumatol. 1987;26:424-429.

44. Forrest JB. The response to epidural steroid injections in chronic dorsal root pain. Can Anaesth Soc J. 1980;27:40-46. 45. White AH, Derby R, Wynne G. Injection techniques for the diagnosis and treatment of low back pain. Spine. 1980;5:78-86. 46. Renfrew DL, Moore TE, Kathol MH, et al. Correct placement of epidural steroid injections: Fluoroscopic guidance and contrast administration. AJNR. 1991;12:1003-1007. 47. White AH. Injection techniques for the diagnosis and treatment of low back pain. Orthop Clin North Am. 1983;14:553-567. 48. Hildebrandt J. Relevance of nerve blocks in treating and diagnosing low back pain—is the quality decisive? Schmerz. (article in German). 2001;15(6):474-483. 49. Simon DL, Kunz RD, German JD, et al. Allergic or pseudoallergic reaction following epidural steroid deposition and skin testing. Reg Anesth. 1989;14:253-255. 50. Covino BG. Clinical pharmacology of local anesthetic agents. In: ­Cousins MJ, et al. ed. Neural Blockade in Clinical Anesthesia and Management of Pain. Philadelphia: Lippincott; 1988:111-114. 51. Braid DP, Scott DB. The systemic absorption of local analgesic drugs. Br J Anaesth. 1965;37:394-404. 52. Cousins MJ, et al. Epidural neural blockade. In: Cousins MJ, Bridenbaugh MJ, Phillip O, et al. eds. Neural Blockade. Philadelphia: Lippincott; 1988:340-341. 53. Cousins MJ. Hematoma following epidural block. Anesthesiology. 1972;37:263. 54. Waldman SD, Winnie AD. Caudal epidural nerve block. In: Waldman SD, ed. Interventional Pain Management. Philadelphia: WB Saunders; 1996:381-382. 55. Derby R, Bogduk N, Kine G. Precision percutaneous blocking procedures for localizing spinal pain. Part 2. The lumbar neuroaxial compartment. Pain Digest. 1993;3:175-188. 56. Dincer U, Kiralp MZ, Cakar E, et al. Caudal epidural injection versus non-steroidal anti-inflammatory drugs in the treatment of low back pain accompanied with radicular pain. Joint Bone Spine. 2007;74(5):467-471. 57. Lerner SM, Gutterman P, Jenkins F, et al. Epidural hematoma and paraplegia after numerous lumbar punctures. Anesthesiology. 1973;39: 550-551. 58. Waldman SD. Complications of cervical epidural nerve blocks with steroids: a prospective study of 790 consecutive blocks. Reg Anesth. 1989;11:149-151. 59. Redekop GJ, Del Maestro RF. Diagnosis and management of spinal epidural abscess. Can J Neurol Sci. 1992;19:180-187. 60. Fraser RD, Osti OL, Vernon-Roberts B. Discitis after discography. J Bone Joint ­Surgery. 1987;69:26-35. 61. Crock H. Practice of Spinal Surgery. New York: Springer-Verlag; 1983. 62. Guyer RD, Collier R, Stith WJ, et al. Discitis after discography. Spine. 1988;13:1352-1354. 63. Fernand R, Lee CK. Post-laminectomy disc space infection. A review of the literature and a report of three cases. Clin Orthop Relat Res. 1986;209:215-218. 64. Lindholm TS, Pylkkanen P. Discitis following removal intervertebral disc. Spine. 1982;7:618-622. 65. Thibodeau AA. Closed space infection following the removal of lumbar intervertebral disc. J Bone Joint Surg Am. 1968;50:400-410. 66. Arrington JA, Murtagh FR, Silbiger ML, et al. Magnetic resonance imaging of postdiscogram discitis and osteomyelitis in the lumbar spine: case report. J Fla Med Assoc. 1986;73:192-194. 67. Modic MT, Feiglin DH, Piraino DW, et al. Vertebral osteomyelitis: Assessment using MR. Radiology. 1985;157:157-166. 68. Szypryt EP, Hardy JG, Hinton CE, et al. A comparison between magnetic resonance imaging and scintigraphic bone imaging in the diagnosis of disc space infection in an animal model. Spine. 1988;13:1042-1048. 69. Schellhas KP, Pollei K. Thoracic disc degeneration: Correlation of MR imaging and discography. Presented at the 8th Annual Assembly of the North American Spine Society. San Diego, CA; oct 14-16. 70. Moore DC, Bridenbaugh LD. Oxygen: the antidote for systemic toxic reactions from local anesthetic drugs. JAMA. 1960;174:842-847.

Complications of Common Selective Spinal Injections: Prevention and Management  47 71. Cory PC, Mulroy MF. Post-operative respiratory failure following intercostal block. Anethesiology. 1981;54:418-419. 72. Falco FJ, Irwin L, Zhu J. Lumbar spine injection and interventional procedures in the management of low back pain. Clin Occup Environ Med. 2006;5(3):655-702,vii-viii. 73. Bous RA. Facet joint injections. In: Stanton-Hicks M, Bous R, eds. Chronic Low Back Pain. New York: Raven Press; 1982:199-211. 74. Thomson SJ, Lomax DM, Collett BJ, et al. Chemical meningism after lumbar facet joint nerve block with local anesthetic and steroids. ­Anaesthesia. 1991;46:563-564. 75. Berrigan T. Chemical meningism after lumbar facet joint block. ­Anaesthesia. 1992;47:905-906. 76. Pawl RP. Headache, cervical spondylosis, and anterior cervical fusion. Surg Annu. 1977;9:391-408. 77. Bogduk N, Marsland A. The cervical zygapophysial joints as a source of neck pain. Spine. 1988;13:610-617. 78. Carron H, Litwiller R. Stellate ganglion block. Anesth Analg. 1975;54: 567-570. 79. Lofstrom J, Cousins MJ. Sympathetic neural blockade of upper and lower extremity. In: Cousins M, ed. Neural Blockade in Clinical Management of Pain. Philadelphia: Lippincott; 1988:461.

80. Malmqvist E, Bengtsson M, Sorensen J, et al. Efficacy of stellate ganglion block: A clinical study with bupivacaine. Reg Anesth. 1992;17:340-347. 81. Sachs BL, Zindrick MR, Beasley RD. Reflex sympathetic dystrophy after operative procedures on the lumbar spine. J Bone Joint Surg Am. 1993;75:721-725. 82. Wallace MS, Milholland AV. Contralateral spread of local anesthetic with stellate ganglion block. Reg Anesth. 1993;18:55-59. 83. Schmidt SD, Gibbons JJ. Postdural puncture headache after fluoroscopically-guided lumbar paravertebral sympathetic block. Anesthesiology. 1993;78:198-200. 84. Sprague RS, Ramamurthy S. Identification of the anterior psoas sheath as a landmark for lumbar sympathetic block. Reg Anesth. 1990;15:253-255. 85. Waldman SD, Winnie AP. Interventional Pain Management. W B Saunders; 1996. 86. Kricun R, Kricun ME. Computed Tomography of the Spine: Diagnostic Exercises. Aspen Publications. 1987. 87. Daffner RH. Clinical Radiology: The Essentials. Williams & Wilkins; 1993.

6

     

Appendix

I

American Heart Association, Advanced Cardiac Life Support (ACLS) Protocols, 2005

49

   

Appendix II: Treatment of Acute Reactions

Urticaria Discontinue injection Diphenhydramine (Benadryl) or hydroxyzine (Vistaril), PO/IM/ IV, 25-50 mg ll Cimetidine PO/IV, 300 mg or ranitidine PO/IV, 50 mg ll If severely disseminated, give epinephrine SC (1:1000), 0.1-0.3 mL ll ll

Facial and laryngeal edema

II

Oxygen via mask, 6-10 L/min* Secure IV access and initiate rapid administration of large volumes, IV, of isotonic Ringer lactate or normal saline solution ll If poorly responsive, atropine, 0.6-1.0 mg, slowly, IV ll Repeat atropine to a total dose of 0.04 mg/kg (2-3 mg) in adult patient ll ll

Hypertension (severe) Monitor vital signs (BP, pulse oximetry, and ECG) Nitroglycerin, 0.4 mg, SL or Nitropaste topical ointment, 1-2 inch ll If persistent, transfer for further evaluation to ER or ICU setting ll For pheochromocytoma, give phentolamine, 5 mg (adults), 1 mg (children) ll ll

Epinephrine SC (1:1000), 0.1-0.2 mL; or if hypotensive, give 1:10,000, slowly, IV, 0.1 mL ll Oxygen via mask/endotracheal tube, 6-10 L/min* ll If resuscitation needed, initiate ACLS protocol and call EMS ll

Bronchospasm

Seizures—convulsions Monitor vital signs (BP, pulse oximetry, and ECG) Oxygen via mask, 6-10 L/min* ll Maintain IV access ll Protect patient from physical injury during seizure ll Insert bite block ll If seizure is longer than 2 minutes, secure airway and oxygenate ll Obtain neurologic consult ll Give diazepam (Valium), 5 mg, IV, or midazolam (Versed) 2.5 mg, IV ll If longer effect needed, consider phenytoin (Dilantin) infusion, 15-18 mg/kg, at rate of 50 mg/min ll Consider ACLS protocol, if intubation is needed ll

Oxygen via mask, 6-10 L/min* ll Monitor vital signs (BP, pulse oximetry, and ECG) ll Beta-agonist inhalers (e.g., albuterol) ll Epinephrine SC (1:1000), 0.1-0.2 mL; or if hypotensive, give 1:10,000, slowly, IV, 0.1 mL ll If oxygen saturations persist <88%, initiate ACLS protocol and call EMS ll

Hypotension with tachycardia Reverse Trendelenburg position Monitor vital signs (BP, pulse oximetry, and ECG) ll Oxygen via mask, 6-10 L/min* ll Rapid administration of large volumes, IV, isotonic Ringer lactate or normal saline solution ll If poorly responsive, epinephrine SC (1:10,000), 1.0 mL, slowly, IV

ll

ll ll

Hypotension with bradycardia—vagal reaction Reverse Trendelenburg position ll Monitor vital signs (BP, pulse oximetry, and ECG) ll

*Always administer supplemental oxygen with caution in a patient with chronic pulmonary disease.

Pulmonary edema Elevate torso; rotating tourniquets (venous compression) Oxygen via mask, 6-10 L/min* ll Diuretics—furosemide (Lasix), 40 mg, IV, slow push ll Consider morphine ll Transfer to ICU or ER setting, for further management ll ll

Prophylaxis for adverse intravascular iodinated contrast media reactions ll ll

Avoid unnecessary exposure to contrast medium Substitute nonionic for ionic contrast medium 51

52  Basic Principles of Procedures

In adults, give prednisone, 50 mg, PO, 12 hrs, then 2 hrs prior to procedure ll Give diphenhydramine (Benadryl), 50 mg, PO, 1 hr prior to procedure ll For pheochromocytoma; give phenoxybenzamine, 10-20 mg, 3-4 times/day, PO, for 7-10 days; or 24 hours prior to procedure, give phenoxybenzamine, 0.5 mg/kg in 250 mL of D5W, slowly, IV, over 2 hrs ll

Dysrhythmias ll

Refer to ACLS protocol

Procedural Documentation and Coding

7

Kim Pollock, RN, MBA, CPC Successful pain management practices have implemented processes and procedures that focus on customer service, physician and staff efficiency, and risk reduction which result in optimizing the revenue cycle. The goal is to ensure that all revenue cycle tasks are performed by the right number of people at the right time with the right tools to collect timely and optimal revenue. The revenue cycle, or the process of getting paid, begins with the patient entering a pain management practice and ends with collection of all collectable dollars associated with the services provided to that patient. Every employee and provider in the practice, from the ­person who answers phones to the pain management professional, has an important role to play in the revenue cycle. Revenue cycle processes can be divided into two types as shown in Table 7-1—the processes performed on the front-end and the processes performed on the back-end. Front-end processes are those that typically are performed with patient involvement, whereas back-end processes are performed without the patient’s involvement or presence. The accuracy of patient information and timely completion of front-end processes drives the success of the back-end processes to ultimately achieve revenue optimization.

Front-End Processes Front-end processes in the revenue cycle include appointment scheduling and preregistration, insurance verification and referral management, check-in, the patient encounter (where coding and documentation occur), test/procedure coordination, and check-out.

Appointment Scheduling Appointment scheduling is typically the practice’s first encounter with the patient and is one of the most critical steps in the revenue cycle. Future third-party billings and collections efforts depend on the quality of the data obtained at this time. Therefore, it is imperative that accurate and complete patient demographic and insurance information be obtained. The appointment scheduling process includes, but may not be limited to, the following tasks: Obtain all patient demographic and referring provider information and enter into the practice management information system (PMIS); this is called preregistration ll Re-register all established patients (e.g., verify or update previously obtained demographic and insurance information) ll Make the appointment, hopefully within patient’s desired time frame ll

Inform the patient of practice’s financial policies including collection of co-payment at the point of service (POS), ll Refer the patient to the practice’s website (if one is available) to download a map, health history form, other patient education materials ll Coordinate or make a reminder phone call to the patient about the appointment and financial policies ll

Successful practices obtain patient demographic information directly from the patient, rather than from the referring physician’s office, to ensure accuracy. Practices that are business savvy offer on their website the ability to make an appointment and provide preregistration demographic and insurance information.

Insurance Verification Insurance verification and referral management can be a separate process, depending on the size of the pain management practice, or it can be performed at the time of appointment scheduling. Practices obtain required managed care referrals and verify the patient’s insurance eligibility and benefits prior to all new patient appointments to ensure appropriate collections on the back-end. Successful practices will reverify insurance benefits on all established patients not in a postoperative global period. All too often a practice finds that a patient, new or established, does not have the insurance coverage he or she claims to have and the practice ultimately is not paid for rendered services. Validation of insurance eligibility and benefits as well as obtainment of referrals for pain management services may be done electronically through on-line capabilities with many payors. It is not always necessary to have this task performed via telephone call requiring staff time. The on-line capabilities come in various formats, such as accessing information directly from a payor’s on-line database or through the PMIS vendor who might perform “batch” (for a group of patients) or “on demand” (for an individual patient) eligibility and benefits verification for the practice. In summary, the goal of the first two steps in the revenue cycle is to gather and verify patient demographic and insurance information prior to the appointment to provide an optimal opportunity to assess the financial risk, verify insurance eligibility, and obtain proper referrals to ensure appropriate revenue collection when the service is provided.

Check-In The receptionist plays an important role in the revenue cycle process by validating the patient’s identity and the previously obtained insurance information, as well as collecting any mandatory 53

54  Basic Principles of Procedures

Table 7-1  The Front-End and Back-End Revenue Cycle Processes Front-End Processes

Back-End Processes

Appointment scheduling and ­pre-registration

Claim/statement production

Insurance verification and referral management

Payment processing and analysis

Check-in

Denials management

Patient encounter

Accounts receivable follow-up

Test/procedure coordination Check-out

copayment. Tasks required at the check-in phase of the revenue cycle include, but are not limited to: Marking the patient as “arrived” in the PMIS so the system “looks for,” or reconciles, a corresponding charge for the service provided ll Scanning the patient’s insurance card into the PMIS (or photocopying for the paper chart) ll Validating the patient’s identity by comparing the name on the insurance card to the name on a government-issued photo identification card to the patient’s actual identity ll Obtaining required signatures on practice forms or electronic documents (e.g., consent to treat, information release) and communicating the projected patient financial responsibility for the service ll Collecting any insurance company mandated co-payment, entering this action in the PMIS, and providing a system-generated receipt to the patient ll

It is imperative that co-payments be collected at the point-ofservice because this is the point at which the patient’s motivation to pay is greatest and the cost of collections is lowest.

Patient Encounter The pain management provider renders a service in the office (e.g., evaluation and management code, radiology code) or a procedural service (e.g., injection code, surgery code) and is responsible for documenting and coding the service so accurate billing can occur. Coding for, and documentation of, services performed is best performed by the rendering provider because these are critical components of the revenue cycle. Coding is typically performed on a paper charge ticket, also called an encounter form, or may be done electronically through the PMIS. CPT Codes Current procedural terminology (CPT) is a set of codes, descriptions, and guidelines intended to describe procedures and services performed by physicians and other health care providers. Each procedure or service is identified with a five-digit code. The CPT manual is updated annually by the American Medical Association (AMA) and the pain management professional specialty societies contribute to CPT code development and maintenance. There are extensive service and procedure coding requirements published in the CPT manual. Providers are responsible for knowing how to accurately report, and document, CPT codes for the services rendered.

There are three categories of CPT codes. Category I CPT codes describe a procedure or service identified with a five-digit numeric CPT code and descriptor nomenclature; these are considered the “usual” CPT codes and are widely accepted by third party payors. Category II codes, five-digit codes with four numbers and ending with the letter “F”, are intended to facilitate data collection on positive health outcomes and quality patient care. Category III codes, five-digit codes with four numbers but ending with the letter “T”, facilitate data collection on and assessment of, new services and procedures and are used to report procedures that do not have a Category I code. Payors require a valid Category I and/or Category III code(s) for payment consideration. The various types of CPT codes are listed in Table 7-2 with a notation of the application to the pain management specialty. ICD-9-CM Codes ICD-9-CM codes classify diseases and a wide variety of signs, symptoms, abnormal findings, complaints, social circumstances, and external causes of injury or disease. These three, four, and five digit diagnosis codes are used to support, or justify, the CPT codes reported by providers. ICD-9-CM codes are published by the World Health Organization (WHO), whereas the annual coordination and maintenance process is jointly controlled by two branches of the United States government—the National Center for Health Statistics (NCHS) and the Centers for Medicare and Medicaid Services (CMS). Audits comparing code(s) selected by pain management providers to the documentation should be performed on a regular basis to ensure compliance with third party payor and AMA guidelines. Regular audits and coding education are important components to a practice’s revenue and compliance success.

Test/Procedure Coordination Many pain management practice patients will require further diagnostic testing and/or diagnostic or therapeutic procedures after seeing a pain management professional. Third party payors often require precertification for testing, such as radiologic procedures, including plain films, magnetic resonance imaging (MRI), and CAT (computerized axial tomography) scans. Successful practices will incorporate this precertification need into the revenue cycle process, particularly if the practice has the capabilities of performing the imaging service. Imaging services performed, and billed, by a pain management professional require the production of a radiologic interpretation report which must be separate from the office visit documentation. Procedural services, such as injections and surgical procedures, also may require precertification prior to performance of the procedure. The procedure coordinator’s duties include, but are not limited to: Reverification of insurance eligibility if significant time has passed since the previous insurance eligibility verification ll Precertification and specific third party benefits information for the service (some payors allow this to be performed on-line) ll Scheduling necessary preprocedure or preadmission testing ll Scheduling the procedure in the designated facility (e.g., ambulatory surgery center, hospital) ll Presurgical financial counseling and collection of a procedure deposit to include the projected patient financial responsibility calculated after obtaining third party benefits information ll

Procedural Documentation and Coding  55

7

Table 7-2  Types of CPT Codes* and Application to Pain Management Category I CPT Codes CPT Code Number

Type of CPT Code

Application for Pain Management

00100-01999, 99100-99140

Anesthesiology

Codes describe administration of anesthesia during procedures (generally surgery CPT codes) performed by another provider/ physician

10021-69990

Surgery

Includes codes for injections, placement of pain pumps, and other pain management diagnostic and therapeutic services

70010-79999

Radiology (including nuclear medicine and ­diagnostic ultrasound)

Includes fluoroscopic guidance and localization of needle or catheter tip for pain management procedures as well as diagnostic radiologic procedures

80047-89356

Pathology and laboratory

These codes are generally not used by pain management providers

90281-99199, 99500-99607

Medicine (except anesthesiology)

Includes nerve conduction and electromyography diagnostic ­testing codes

99201-99499

Evaluation and management

Includes codes for office visits, consultations, and hospital visits used by pain management providers Category II CPT Codes

0001F-7025F

These codes are supplemental tracking codes that can be used for performance management. They are intended to facilitate data collection about quality of care rendered; the use of these codes is optional.

0016T-0196T

These codes are used to report temporary codes for emerging technology, services, and procedures and are used instead of an unlisted Category I CPT code (e.g., 64999).

Includes codes for oncologic pain management as well as ­assessment and examination of back pain

Category III CPT Codes Includes code for percutaneous intradiscal annuloplasty

*As per CPT 2009.

Procedure/surgery charge entry (or this may be done on the back-end) ll Reconciling the procedure scheduling log to ensure all charges are received from the rendering pain management professional ll

Check-Out After the office encounter is complete, successful practices have incorporated at the point-of-service the task of collecting from the patient any estimated co-insurance, unmet deductible, as well as any previously unpaid balance. Alternatively, previously unpaid balances may be collected during the check-in process. Like collection of co-payments at check-in, collecting patientresponsible portions of the service charge will result in optimal collections and a reduction in expense for patient statement production. Additional duties performed at check-out include, but are not limited to: Scheduling follow-up appointment to avoid delayed follow-up or accessibility problems ll Checking for unanswered questions and additional service opportunities ll Checking service to ensure the patient’s experience was good ll Posting charges for the service(s) rendered as well as any payments and generating a receipt from the PMIS ll Reconciling “arrived” patients to provider completed charge tickets/encounter forms received to ensure a charge is received for each patient seen that session ll

The best time to collect from a patient is at the point-of-service on the front-end where there is direct patient contact.

Back-End Processes Back-end processes in the revenue cycle include claim/statement production, payment processing and analysis, claim denials management, and accounts receivable follow-up.

Claim and Statement Production Professional claims to third party payors can be sent electronically or on paper (also known as hard copy) using a CMS 1500 health insurance claim form. Successful practices submit accurate electronic claims on a daily basis to as many payors as possible; some payors, such as many worker’s compensation plans, require paper claims. Payors tend to process electronic claims in a more timely manner, which helps pain management practices improve cash flow and keep the accounts receivable low. Table 7-3 includes seven very important tips for successful claim submission. The goal is to submit only once a “clean” claim, meaning one without errors or omissions, and be paid in a timely manner. Practices typically send third party payor claims to a clearinghouse for review, or “scrubbing”, to ensure the demographic, insurance, and code information is appropriate prior to the claim being sent to the insurance company. The edit report, or list of errors noted on the submitted claim, received by the practice must be rectified on a daily basis.

56  Basic Principles of Procedures

Table 7-3  Tips for Successful Claim Submission ll

ll

ll

ll ll

ll ll ll ll

ll

Enter the patient’s name as it appears on the insurance benefits card. Watch for patients using their middle name as a first name and be sure to enter initials. Enter patient or payor identification numbers with proper prefixes and/or suffixes. Correlate CPT code(s), in box 24D, to the corporate ICD-9-CM code(s) listed in box 21 on the claim form. Report CPT codes in descending value order—the highest listed first. Enter bilateral procedures, using modifier 50, either on one line (called the “bundled” format) or on two lines (“line-item” format) as noted below. Check with payors for format preference of bilateral procedures to ensure appropriate reimbursement. Bundled format Line-item format 64475-50 1 unit Double fee 64475 1 unit Single fee 64475-50 1 unit Single fee List the name and national provider identification number (NPI) of the provider requesting the consultation in boxes 17, 17A, and 17B of the CMS 1500 health insurance claim form. Generally box 23 is used for referral, authorization, or precertification numbers, although some plans may use box 19 instead. Check with individual payors for preference.

Patients are sent statements on a periodic basis, usually monthly, showing the balance owed to the provider. The first statement should be sent, if a patient balance exists, immediately on the practice’s receipt of a third party payment. Patient statements may be generated by the PMIS or outsourced to a third party for processing and mailing. Again, it is important to collect as much from patients at the time of service (office or procedure) to avoid the expense of sending a statement after the service is rendered.

Payment Processing and Analysis Payments from third party payors and patients come to the practice in various ways including: Mailed directly to the practice Mailed to a bank lockbox ll Electronically paid using the practice’s website capabilities ll Electronically paid to the practice’s bank account (also known as electronic funds transfer, or EFT). ll ll

Third party payor payments are usually accompanied by an explanation of benefit (EOB) form that describes the payor’s payment or nonpayment of services submitted. Specific EOB information necessary for analysis includes, but is not limited to: Payment amount Contractual allowances ll Co-payment, deductible, and co-insurance amounts (e.g., patient financial responsibility) ll Rejection or denial codes ll ll

The practice should expect to receive an EOB for every service submitted to a third party payor. EOBs may be received on paper or electronically, called electronic remittance advice (ERA). Many payors will show their payment by “line item,” or by each CPT code billed. Yet, others lump services as medical services or surgical services. When the latter happens, the practice’s staff must contact the payor to determine how to allocate in the PMIS all payments for each service and determine that the payment is correct.

Efficient practices receive as many electronic payments, and EOBs, as possible to decrease human resource expense for posting payments and EOB information into the PMIS. Payment posting into the PMIS and analysis of the payment and EOB must occur to: Ensure the practice was paid according to the third party ­contract terms ll Focus on trends where services are denied for the following reasons: inappropriate bundling, medical necessity, low-pay appeals, incorrect coding, and inappropriate reporting of services during the global period ll Track the following rejections to identify front-end processrelated problems: ll demographic errors ll eligibility-related denials ll wrong primary/secondary insurance company ll no referral authorization ll no coverage at time of service ll

Appropriate analysis of each EOB is critical because the data elements on the EOB drive the next steps in the revenue cycle— whether to bill a secondary third party payor for any balance or send a statement to the patient for payment of the balance. Another important aspect of EOB analysis is to determine any primary third party claim follow-up course of action such as a denial appeal or internal practice process change to avoid future denials. The pain management professional should be involved in denial appeals for medical necessity and coding denials.

Accounts Receivable Follow-Up Some third party payors reimburse pain management professionals in a timely manner. For example, Medicare reimburses a provider within 14 days of a clean electronic claim, whereas other payors may take weeks to months to reimburse. Unpaid charges or claims, called accounts receivable (A/R), should be monitored in 30-day increments. For example, “current” A/R is 0 to 30 days from the date of service, whereas older charges are measured in 31 to 60, 61 to 90, and greater than 90-day increments. Older charges, whether the responsibility of a third party payor or a patient, are generally more difficult to collect. The best opportunity for a pain management practice to collect from the patient is while the patient is in the office or facility. It is essential that pain management practices have an organized methodology implemented for monitoring and follow-up on unpaid balances. Occasionally, a pain management practice may need to send an unpaid balance to a collection agency or take legal action for payment. It is imperative that the rendering pain management professional, rather than billing staff or the office manager, be responsible for making the decision to pursue a formal outside collections process.

Conclusion A successful revenue cycle involves efficient, cost-effective, compliant, and accurate processes on the front-end as well as backend of a pain management practice’s operations to achieve optimal collections for rendered services.

8

Medicolegal Issues Julie K. Silver, MD, and Susan M. Donnelly Murphy, JD

Physicians who routinely perform pain procedures need to understand certain elements of informed consent to minimize their risk of medicolegal entanglements. Often physicians have little or no training in obtaining informed consent. Even when they do obtain training, the instruction may be incomplete or incorrect. Understanding and documenting the consent process before the procedure is as important as the procedure itself.

Understanding Informed Consent The law implicitly recognizes that a person has a strong interest in being free from nonconsensual invasion of bodily integrity.1 In short, the law recognizes the individual’s interest in preserving the “inviolability of the person,”1 an interest protected within the context of medical malpractice with the doctrine of informed consent. It has long been accepted that a patient must agree to any procedures or treatment. However, earlier it was accepted that the physician could steer the patient in the direction that he or she wanted. This has changed: it is now recognized that “[I]t is the prerogative of the patient, not the physician, to determine the direction in which his … interests lie.”1 Consequently, a body of law that dictates the manner in which the patient’s consent or refusal needs to be obtained has developed. Some consider the right to informed consent to be the most important aspect of patients’ rights.2 If patients are to intelligently exercise control of their bodies and attendant medical care, they must be provided with appropriate and complete medical information on which to base their decision. The dilemma facing medical practitioners is the determination of when such informed consent needs to be obtained and the manner in which to obtain it. This requires knowledge of the type and extent of information to be given to an individual patient and the manner in which it is to be presented. Although the vast majority of claims of medical malpractice focus on errors in diagnosis and improper treatment and performance of procedures, a recent analysis found that allegations of failure to inform and breach of warranty were present in 6% of cases.3

The Legal Framework for Informed Consent Complete informed consent should be obtained for all therapeutic and diagnostic procedures. Any course of treatment that carries with it the risk of permanent injury requires a full disclosure before consent. Full informed consent should precede medical treatment

even for procedures with a risk of temporary injury alone. Only under emergency conditions or in situations in which there are no therapeutic options should informed consent be omitted. There is no excuse to fail to obtain informed consent for an elective procedure. The physician performing the procedure is the appropriate person to meet with the patient. Of course, other health care providers are of great assistance to reaffirm the consent, answer additional questions a patient may have, and continue a dialogue. To enable a patient to make an informed decision, “the physician owes to his patient the duty to disclose in a reasonable manner all significant medical information that the physician possesses or reasonably should possess that is material to an intelligent decision by the patient whether to undergo a proposed procedure.”1 The specific law varies somewhat from jurisdiction to jurisdiction. Use of this language facilitates discussion of the two perspectives involved in the decision-making process: the physician and the patient.

Role of the Physician The major role of the physician in the process of obtaining informed consent is that of an expert. Through education and experience, the physician is able to recognize the risks and benefits of the proposed treatment. Because the patient has limited knowledge of the medical and technical aspects of the procedure, the physician should begin the discussion with a reasonable explanation of the medical diagnosis—an obvious but often overlooked point. Thereafter, significant information includes the nature and probability of risks involved in the procedure, expected benefits, the irreversibility of the procedure, the available alternatives to the proposed procedure, and the likely result of no treatment.1 Whether a physician has provided appropriate information to a patient generally will be measured by what is customarily done or by the standard of what the average physician should tell a patient about a given procedure. It often is essentially the same information that the physician has imparted to countless previous patients. In general, the duty to disclose does not require the physician to disclose all possible and/ or remote risks, nor does it require the physician to discuss with a patient the information that he believes the patient already has, such as the risk of infection or other inherent risks of a procedure.1 Recent studies have focused on the manner in which informed consent is obtained. For example, in a prospective, randomized, controlled study conducted by Bennet and colleagues, 99 out of 109 patients undergoing imaging-guided spinal injections agreed to 57

58  Basic Principles of Procedures

particpate and were assigned to one of three groups.4 The control group was given informed consent in the customary manner at the investigators’ institution with 12 key points of consent discussed conversationally. The “teach-the-teacher” group had to repeat the 12 key points back to the investigator before informed consent could be completed. The third group viewed a set of diagrams illustrating the 12 key points before signing the informed consent. Following the procedure, all participants completed a survey to test knowledge recall, anxiety, and pain during the procedure. Statistically significant results included a lower survey score for the control group. Not surprisingly, it took significantly longer to obtain informed consent in the “teach the teacher” group than in the control group or in the diagram group. Overall, the diagram method was optimal and required less time and had improved patient-physician communication. The manner in which information is given and how much information is offered, are both important considerations. Too much information may actually increase anxiety just prior to a procedure.5 A recent review on informed consent in Pain Practices found that although “disclosure has improved, but is still uneven, comprehension is often poor, for both patients and research subjects.”6 An important factor is not only the improvement of consent forms, but also improving the consent process. A group of Swiss researchers studied the effect of combined written and oral information versus just oral information when obtaining informed consent. In this study, participants who were given the written information as well as the oral instructions rated the quality of information they received as higher than the oral-only group.7

Role of the Patient Although explanations to patients may be nearly identical for a given procedure, the law often also requires that the conversation be tailored to the particular patient. It is incumbent on the physician to have an appreciation of what information is important to a particular patient. The patient has the right to know all information that he or she considers material to his or her decision. Materiality is defined as the significance a specific patient attaches to the disclosed risks in deciding whether to undergo the proposed procedure.8 Materiality of information about a side effect or consequence is a function not only of the severity of that consequence, but also of the likelihood that it will occur.8 Remote risks whose likelihood of occurrence is not more than negligible need not warrant discussion. In summary, provide the patient with a realistic appreciation of his or her medical condition and an appropriate explanation of the treatments available. Never forget that however unwise his or her sense of values may be in the eyes of the medical profession, every patient has the right to forgo treatment or even cure if it entails personally intolerable consequences or risks.8

Avoiding Legal Entanglements Lack of informed consent may develop into a lawsuit only when a physician fails to disclose a risk that subsequently becomes an injury. Otherwise, as one court stated, “an omission (of material information), however unpardonable, is legally without consequence.”9 Practically, the patient must demonstrate that, had the proper information been disclosed, he or she would not have consented to the course of therapy. To control the subjectivity of this application, some jurisdictions require the patient to prove that if

the risk had been disclosed neither this patient, nor a reasonable person in this patient’s situation, would have consented.1

Requirements of Documentation A signed form entitled “consent to treatment” is required for all procedures; note, however, that the form only proves consent, not that it was informed.10 The exchange of information that precedes the signed consent is crucial to the process. Good chart documentation (including signed consent forms, which are often and appropriately recommended by attorneys and risk managers) does not insulate a physician from a lawsuit but does make the defense of one considerably less difficult. Malpractice claims often are made years after the treatment was rendered, by which time any specific discussion with the patient in question has long since faded from memory. A standard consent form does nothing to jog the memory of the physician or the patient about the discussion; thus, it is highly important to tailor the discussion (and the subsequent documentation) for each patient, regardless of the procedure. Gone are the days when the phrase “reviewed the risks and benefits and the patient consents” was sufficient. On the standard consent form there usually is an area in which additional information may be added—savvy doctors will make pertinent notes in this body before every procedure (Fig. 8-1). For example, if trigger-point injections are to be given in the piriformis muscle, note that injury to the sciatic nerve is possible. If the injections are to be done in the region of the middle trapezius, noting that potential complications include a pneumothorax is more appropriate. Any notations on the consent form may be bolstered by further documentation in the medical record regarding the details of the discussion. In certain circumstances, it may be advisable to provide the patient with a written summary of the discussion to take home and review before the procedure. It is also advisable to document concerns that the patient expressed and how these concerns were addressed. Finally, note all persons present for the discussion, including other health care providers or individuals who accompanied the patient. If possible, have one of the additional medical persons present for the discussion also sign the consent form. This person can subsequently be available to the patient for further information, and, should there be an adverse outcome, this person can attest to the completeness of the consent discussion.

The Role of the Doctor-Patient Relationship In studies that have explored the relationship between physicians’ claims experience and the quality of care they provide, a common theme is that the differences between sued and never-sued physicians are not necessarily explained by their quality of care or their chart documentation. “[I]f quality of care, medical negligence, and chart documentation are not the critical factors leading to litigation, what factors are critical? Patient dissatisfaction is critical.”11 Although the law dictates what needs to be said to a patient, experience dictates that the manner in which it is said and the amount of time it takes to say it are equally important in providing good quality care and in avoiding a malpractice allegation. Effective communication between the patient and the physician not only enhances treatment outcomes but also enhances patient satisfaction. This combination tips the balance away from litigation, even in the face of unfavorable procedure outcomes.

Medicolegal Issues  59

8

Figure 8-1  Sample consent form.

One study found that routine visits with physicians with no malpractice claims were longer than routine visits with physicians who had experienced malpractice claims.11 This same study found that the malpractice claims were more strongly correlated with the process and tone of a discussion than the content of that discussion.

When Medical Negligence Is an Issue Full and complete informed consent is never a substitute for competent medical care. Claims arising exclusively under the doctrine of informed consent assume that the treatment was rendered appropriately and that a known and accepted risk occurred in the absence of negligence. When the procedure was not performed appropriately, there is a basis for the additional (and more common) claim for medical negligence. By virtue of the doctor-patient relationship, a physician must exercise the degree of knowledge and skill of the average qualified physician practicing the specialty.12 Any breach of this standard that results in injury to a patient may be actionable as a medical malpractice claim. Proof of compliance with the standard of

practice usually will come through a review by an expert witness, who will offer opinions based on his or her education, training, and experience in the specialty, and, in particular, in the procedure at issue. In addition, an expert opinion must be based on the facts of the case. The medical records best demonstrate facts. It is essential to accurately and completely describe every procedure. The procedure note should contain the indications for the procedure, the details of its performance, and the patient’s reaction or initial outcome. For example, the diagnosis for a trigger-point injection may be fibromyalgia, and the indications may be to alleviate pain and muscle spasm. Symptoms and their duration and prior treatment intervention also should be documented. The following sample documentation may be useful: “Under sterile conditions using a 1-inch, 27-gauge sterile disposable needle and a solution of 2 mL 1% lidocaine (Xylocaine) and 10 mL 0.25% bupivacaine (Sensorcaine), a total of 6 trigger-point injections were done in the bilateral upper trapezii. A 2 mL aliquot of the mixture was used at each site. Patient tolerated the procedure well and reported immediate relief of pain in the cervical region.” Finally, follow-up plans should be clearly documented. Once again, providing the patient with a copy of the plan may be appropriate.

60  Basic Principles of Procedures

After analysis of the records, an expert may evaluate the physician’s proficiency with the procedure. “When a new procedure is instituted into clinical practice, proctorship and supervision by a more experienced colleague or other specialist with appropriate documentation may help establish a basis for indicating that the physician has attained the requisite degree of knowledge and skill for the procedure.”13 In conclusion, informed consent involves explaining the diagnosis to the patient in language that he or she understands, possible treatment options, and the risks and benefits of the proposed treatment (procedure). Thoroughly documenting informed consent in an individualized manner is imperative. Improving the process by using written and oral instructions, as well as diagrams, may be helpful. REFERENCES   1. Harnish v Children’s Hospital Medical Center, 387 Mass. 152, 439 N.E.2d, 240 (1982).   2. Annas GJ. A national bill of patients’ rights. N Engl J Med. 1998;338: 695-699.   3. Physician Insurers Association of America: Cumulative Data Sharing Reports, 1997.

  4. Bennett DL, Dharia CV, Ferguson KJ, Okon AE. Patient-physician communication: informed consent for imaging-guided spinal injections. J Am Coll Radiol. 2009;6:38-44.   5. Yucel A, Gecici O, Emul M, et al. Effect of informed consent for intravascular contrast material on the level of anxiety: How much information should be given? Acta Radiol. 2005;46:701-707.   6. Cahana A, Hurst SA. Voluntary informed consent in research and clinical care: An update. Pain Pract. 2008;8:446-451.   7. Felley C, Perneger TV, Goulet I, et al. Combined written and oral information prior to gastrointestinal endoscopy compared with oral information alone: A randomized trial. BMC Gastroenterol. 2008;8:22.   8. Precourt v Frederick, 395 Mass. 689, 481 N.E.2d 1144 (1985).   9. Cobbs v Grant, 8 Cal. 3d 229, 104 Cal. Rptr. 505, 502 P. 2d 1 (1972). 10. Urbanski PK. Getting the “go ahead”: Helping patients understand informed consent. AWHONN Lifelines. 1997; 1(3):45-48. 11. Levinson W, Roter DL, Mullooly JP, et al. Physician-patient communication: The relationship with malpractice claims among primary care physicians and surgeons. JAMA. 1997;277:553-559. 12. Brune v Belinkoff, 354 Mass. 102, 235 N.E.2d 793 (1968). 13. Brenner RJ. Interventional procedures of the breast: Medicolegal ­considerations. Radiology. 1995;195:611-615.

Upper Extremity Joint ­Injections

9

Ted A. Lennard, MD Intraarticular injections with corticosteroids and anesthetic can be a useful treatment option for patients with disabling peripheral joint pain. The anesthetic injected can provide useful diagnostic information and help determine a patient’s pain generator. These forms of injections are performed in conjunction with a comprehensive treatment program. This chapter will review common indications for intraarticular corticosteroid injections, dosing of medications injected, and discuss the technique for upper extremity intraarticular joint injections.

Indications for Intraarticular Steroids The most common use of corticosteroids in the peripheral joints is in patients with rheumatoid arthritis.1 These drugs are used specifically to reduce inflammation and provide relief from pain attributable to synovitis and conditions associated with rheumatoid arthritis. Other indications for the use of corticosteroids into joints include painful osteoarthritis and adhesive capsulitis. Aspiration of synovial fluid for pain relief and laboratory evaluation of the synovial fluid and arthrography for the evaluation of joints are common diagnostic tools that facilitate the rehabilitation of painful joints.

Drugs: Action, Selection, Dosage Corticosteroids produce significant antiinflammatory effects. Numerous long-acting corticosteroid ester preparations are available. The most widely used corticosteroids include triamcinolone acetonide (Kenalog), triamcinolone hexacetonide (Aristospan), betamethasone sodium phosphate (Celestone) and betamethasone acetate (Soluspan), and methylprednisolone acetate (Depo-Medrol).2 These compounds were developed to reduce undesirable hormonal side effects with less rapid dissipation from the joint. None of these corticosteroid derivatives appears to have any superiority over another; however, triamcinolone hexacetonide is the least watersoluble preparation and thus provides the longest duration of effectiveness within the peripheral joint space.3 Systemic absorption after peripheral joint injection occurs within 2 to 3 weeks. Improvement of inflammatory processes remote from the injection site demonstrates that intraarticular corticosteroids exert a systemic effect. The pharmacology of corticosteroids and anesthetics is discussed in Chapter 2. Estimated dosages for the peripheral joints vary widely and usually depend on the size of the joint. The larger joints, such as the knee and shoulder, respond well to a 40-mg dose of methylprednisolone

acetate or the equivalent of another agent. The smaller joints, such as the elbow and ankle, respond to a 20- to 30-mg dose of methylprednisolone acetate or the equivalent. Even smaller joints, such as the acromioclavicular and sternoclavicular joints, respond to a 10- to 20-mg dose of methylprednisolone acetate or the equivalent. The number of injections per joint is also widely variable. Commonly, joints that are injected for the purpose of reducing inflammation in rheumatoid arthritis will be injected many times over the course of the disease process. These multiple injections have been shown to cause interference with normal cartilage protein synthesis.2 However, it has also been demonstrated that patients with long-standing rheumatoid arthritis who do not receive intraarticular corticosteroid injections have joint disuse and decreased function much sooner than those who receive the injections.4 For the purposes of pain reduction in osteoarthritis as well as an adjunct in the mobilization of the treatment of adhesive capsulitis, injections at the rate of one per 4 to 6 weeks for a maximum of three injections is the most commonly accepted regimen. This regimen, of course, is subject to the patient’s response to his or her overall treatment plan, of which the intraarticular corticosteroid injection is but one part. It is usual practice to combine the corticosteroid medications with an anesthetic substance, such as procaine (Novocain) or lidocaine (Xylocaine) or the equivalent. The combined use of corticosteroids and anesthetic agents provides a larger volume of injectable material with which to bathe the joint more adequately. The added effect of analgesia is also desirable for patient comfort and for a more immediate response to treatment. Thus, the patient may obtain immediate pain relief and provide valuable feedback with which to help determine the overall rehabilitation plan. The usual anesthetic injected is lidocaine, 1% without epinephrine, with which the practitioner can provide a preliminary skin wheal and a control test before proceeding with the deeper injection. Bupivacaine (Marcaine, Sensorcaine), 0.25% or 0.5%, is also useful in providing a longer-acting analgesic effect for the patient. The dosages of lidocaine and bupivacaine also vary widely with the size of the joint. Usually, the smaller joints such as the acromioclavicular, sternoclavicular, and elbow joints would take 1 to 2 mL of 1% ­lidocaine combined with the corticosteroid. The glenohumeral, knee, and hip joints would take 2-4 mL of anesthetic agent. Bupivacaine is often preferable for non–weight-bearing joints such as the shoulder, elbow, acromioclavicular, and sternoclavicular joints, so long as these joints can be somewhat immobilized for several hours. Likewise, lidocaine is the drug of choice for injections in the weight-bearing joints, such as the knee, because its duration is much shorter and, thus, the joint is subject to less postinjection trauma by the seemingly compliant patient. 63

64  Soft Tissue and Joint Injections

Contraindications and Complications The clinician must be acutely sensitive to contraindications and complications of intraarticular corticosteroid therapy.1,4,5,7,22,26 Some of the most obvious contraindications include infection of the joint or of the skin overlying the joint. A patient with generalized infection also should be considered an unsuitable candidate for corticosteroid injection. Injection of corticosteroids may render a joint susceptible to hematogenous seeding from more distant skin lesions. Thus, the overall health of the patient must be assessed before considering the use of intraarticular corticosteroids.6 Other obvious contraindications include hypersensitivity to any of the anesthetic preparations or the corticosteroids themselves. Patients receiving intraarticular injections in the presence of anticoagulants would be susceptible to bleeding. Determination of prothrombin time is suggested before injection therapy in these patients. Patients with a recent injury to the joint such as a ligamentous destruction or bony destruction of the underlying joint should not be subjected to corticosteroid therapy. Instead, aspiration of the joint may be indicated if there is a relatively large inflammatory effusion.7 Soft tissue or bony tumors at or near the underlying joint would also be a major contraindication to corticosteroid injections. Even small doses of corticosteroids with intraarticular injections may trigger episodes of hyperglycemia, glycosuria, and even electrolyte imbalance in patients with diabetes; caution must be exercised in such situations.8 Although rare, infections can be a serious complication.9,10 Usually, infections can be avoided by using an aseptic technique.11 Infections may be quite subtle in patients with long-standing rheumatoid arthritis and in those receiving immunosuppressive agents. The most common organism is Staphylococcus aureus.12,13 One must also use caution in geriatric patients and in those with debilitating diseases. Hypercorticism from systemic corticosteroid therapy may be a complication if the patient receives multiple intraarticular injections in succession or if the patient is receiving concomitant oral cortisone therapy. Corticosteroid arthropathy with avascular necrosis also has been reported14 but is rare and has not been noted to occur after single corticosteroid injections. Joint capsule calcification is also a potential complication of multiple intraarticular corticosteroid injections.15 Depigmentation and subcutaneous fat necrosis occasionally occur. The depigmentation is cosmetically unacceptable, especially in individuals with darker skin in whom it can be quite noticeable. Fat necrosis usually is not a complication in superficial joints that have minimal amounts of overlying fat tissue. Using a small amount of lidocaine to flush the needle to avoid leaving a needle track of corticosteroid suspension will help to minimize this complication. A common complication in patients with rheumatoid arthritis who are receiving corticosteroid injections in the joints is “postinjection flare” (the joint appears inflamed or even infected), which tends to subside spontaneously in 24 to 72 hours.16 Other less common complications include Tachon syndrome (intense dorsal spine pain immediately following an injection that quickly subsides)17 and chorioretinopathy.18

Alternatives to Corticosteroids Alternatives to intraarticular corticosteroids include viscosupplementation and plasma-rich platelet (PRP) injections. Viscosupplementation injections use gel-like substances such as hyaluronates

to supplement the viscous properties of synovial fluid and have been approved for use in the knee joint. Other joints including the shoulder have been treated with this form of injections with good results.19,20 Plasma rich platelet injections use concentrated platelets from autologous blood to stimulate a healing response in damaged tissue. Blood is drawn from the patient and placed in a centrifuge. The concentrated platelets are removed and reinjected directly into the patient’s abnormal joint, usually under ultrasound guidance. These concentrated platelets produce growth factors that include platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and transforming growth factor-beta (TGF-β). These compounds are instrumental in attracting cells that promote healing by stimulating neovascularization and cellular reproduction.16,21-23 The efficacy of PRP injections and appropriate clinical indications (when and where it should be used) are currently being researched and yet to be definitively determined. Initial results of clinical studies appear promising.24-26

Techniques for Intraarticular Injections When the clinician has established that a peripheral joint needs to be injected or aspirated, the specific preparation for the injection is essentially the same for all joints. Thorough understanding of the underlying anatomy is important to accomplish a painless injection. The optimal site for injection of the joint usually is the extensor surface at a point where the synovium is closest to the skin. Approaching the joint from the extensor surfaces allows the injection to be as remote as possible from any major arteries, veins, and nerves.27 When the site of injection has been determined, it can be marked with the needle hub or a retracted ballpoint pen by pressing the skin to produce a temporary indentation to mark the point of entry. The skin is then prepared by cleansing a generous area with a detergent or cleaner such as an iodine-based surgical scrub. This area is then painted with an antiseptic solution and allowed to dry. Aseptic technique is always advised, including the wearing of sterile gloves so that the area to be injected may be continually palpated and the anatomy appreciated throughout the procedure. A small skin wheal may then be raised using 1% lidocaine with no epinephrine (or an equivalent anesthetic agent). A 27-gauge skin needle approximately 0.75 to 1.0 inch long is used with approximately 1 mL of anesthetic agent. For joints distended with fluid or those that are particularly close to the surface of the skin, such as the acromioclavicular and sternoclavicular joints, the raising of a skin wheal or preanesthesia is usually not necessary. If a patient is particularly apprehensive about the injection procedure, one of the vapo-coolant sprays such as dichlorotetrafluoroethane or ethyl chloride may provide adequate anesthesia. After the skin wheal is raised, a 25- or 22-gauge needle approximately 1.5 inches long may be used to introduce the injectant. The needle is then slid gently into the joint, with the clinician avoiding a strong thrusting motion. Just before beginning the actual injection, the practitioner should aspirate to ensure there is no return of blood. After ascertaining the needle’s positioned in the joint space, the injectable material should be introduced using slow, steady pressure on the plunger. If the joint is to be aspirated before introduction of a corticosteroid, the same technique is used in preparation; however, a larger needle may be introduced, such as a 20- or even an 18-gauge

Upper Extremity Joint Injections  65

needle. Again, slow, steady pressure is used when the needle is introduced into the joint. The aspirate is then withdrawn with the practitioner gently pulling the plunger on the syringe with the dominant hand, holding the syringe barrel steady with the nondominant hand. If it is suspected that not all of the aspirate has been obtained from the joint, the needle tip may be moved around within the joint, and the joint itself may be “milked,” using steady pressure with the opposite hand on the joint itself by kneading the skin toward the site of aspiration. After all of the available fluid is aspirated, the needle may be left in place with the syringe removed. A separate syringe may then be attached to the aspira­ ting needle, and the injectant may then be introduced into the joint itself. Again, a slow, gentle introduction of the injectable material is desired. If resistance is met during the time of the injection, the needle should be readjusted so that there is no resistance. Any time the needle is readjusted, the plunger on the syringe should be withdrawn to ensure that the needle tip does not pierce a blood vessel. After the drug or drugs have been injected, the needle is withdrawn and mild pressure is applied with a sterile gauze pad to prevent bleeding. Whenever the injected material includes corticosteroids, a slight amount of lidocaine may be used to clear the needle before withdrawal. As mentioned earlier, this technique prevents leaving a steroid track through the adipose tissue and skin, which may cause depigmentation or subcutaneous necrosis. Psychological care of the patient is important to the success of these injections. Throughout the procedure, the patient must be coaxed to achieve muscle relaxation and reassured of the importance of the procedure. It is likewise important that the patient be reminded of the practitioner’s skill with and knowledge of the procedure. After the procedure, the patient should be assessed carefully to be sure that he or she is not exhibiting a vasovagal response and that appropriate measures are taken to prevent any secondary harm, such as falling as a result of transient hypotension.

Acromion

Upper Extremity Joints Glenohumeral Joint The glenohumeral joint is subject to multiple traumatic and pathologic problems more frequently than any other joint except the knee. The anatomy of the shoulder must be well understood for a relatively painless injection to be achieved.40 In entering the subacromial space in the shoulder, there is little anterior space for placement of the needle. A lateral or posterior approach may be more desirable.28 When injecting the shoulder for problems such as bicipital tendinitis, the anterior approach is necessary (Fig. 9-1). The patient is placed in a sitting position, the anterior portion of the shoulder is prepared aseptically, and, if desired, a cutaneous wheal is raised medial to the head of the humerus and just inferior to the tip of the coracoid process. It is useful to have obese patients lie supine with the forearm across the abdomen. In this position, the shoulder may be passively rotated internally and externally to identify the head of the humerus. The coracoid process is then easily palpated. The needle is directed in the anteroposterior plane just lateral to the coracoid process. The needle is advanced into the groove between the medial aspect of the humeral head and the glenoid. No resistance should be felt as the needle is advanced. The lateral approach to injection of the shoulder is sometimes useful when treating supraspinatus tendinitis (see Fig. 9-1).28 The patient is placed in a sitting position with the arm relaxed in the lap, which increases the subacromial space. The lateral-most point of the shoulder is palpated and the needle is prepared for insertion below the acromion. After aseptic preparation, the needle is directed almost perpendicularly to the skin surface, with a slight upward angle. The space is then easily entered, and no resistance should be felt as the needle is advanced. The posterior approach to the shoulder is popular for conditions such as adhesive capsulitis as well as synovitis or chronic

Clavicle

Humerus

A

B

C

Figure 9-1  Diagram depicting needle placement for an anterior and lateral glenohumeral joint injection. (A) Surface landmarks for lateral (B) and anterior (C) entry points for injection.

9

66  Soft Tissue and Joint Injections

osteoarthritis (Fig. 9-2).29 The posterior approach also allows the practitioner to be out of the patient’s vision, thereby reducing any apprehension. The patient is placed in the sitting position with his or her arm in the lap, which allows internal rotation of the shoulder and adduction of the arm. The skin is prepared aseptically, and the site of injection is palpated. The site of injection is just under the posteroinferior border of the posterolateral angle of the acromion. It is useful for the practitioner to palpate the patient’s coracoid process in the anterior portion of the shoulder with the index finger. This is the point at which the needle is “aimed.” The needle is then inserted approximately 1 inch below the posterolateral acromion process and directed from the posterolateral portion of the shoulder to the anteromedial portion of the shoulder toward the coracoid process. If resistance is encountered, the needle may be withdrawn

slightly and angled upward. The needle will then be in the upper recess of the shoulder joint away from the head of the humerus.

Acromioclavicular Joint The acromioclavicular joint is small and superficial (Figs. 9-3 and 9-4). It is occasionally swollen and usually tender during palpation when inflamed. This joint can be injected easily using a 25-gauge needle with the patient sitting or supine and the shoulder propped on a pillow. Usually, injections into this joint are for chronic pain, such as occurs in shoulder separations that have not responded to noninvasive treatment. Many times, the joint is injected for diagnostic purposes to delineate the source of pain in the shoulder, and therefore

Clavicle Acromion Spine of scapula Scapula

B

Humerus

A

Figure 9-2  Diagram depicting needle placement for a posterior glenohumeral injection (A). Surface landmarks for posterior injection (B).

Clavicle Acromion

Humerus

A

B Figure 9-3  Acromioclavicular (AC) joint injection (A) with surface landmarks (B).

Upper Extremity Joint Injections  67

corticosteroids are not used. However, with chronic pain that does not subside after a trial of anesthetics (such as lidocaine), corticosteroids may be used. The joint is prepared aseptically, as described earlier. The joint is easily palpated by locating the tip of the distal clavicle and injecting from either a superior angle or an anterosuperior angle into the joint space. In a degenerative joint, many times the needle will not pass easily into the joint, which then needs to be probed gently so that the needle can be advanced just to the proximal margin of the joint’s surface. It is usually not necessary to penetrate the joint any deeper.

Sternoclavicular Joint The sternoclavicular joint is easily located just lateral to the notch of the sternum (Fig. 9-5). Many times the sternoclavicular joint is slightly dislocated, providing a source of pain and making it easily

A C

Figure 9-4  Oblique ultrasound image of the acromioclavicular joint. A, Acromion; C, Clavicle; Arrows, AC joint space; Arrowhead, Fibrocartilaginous disk. (From Jacobson J: Fundamentals of Musculoskeletal Ultrasound. Philadelphia, Saunders, 2007, p 45.)

palpable because the proximal clavicle may be slightly elevated in relationship to the sternum. This joint is small and may be difficult to inject unless a 25- or 27-gauge needle is used. Great care should be taken that these injections into the sternoclavicular area are done superficially because immediately posterior to the sternoclavicular joint are the brachiocephalic veins.

Elbow The elbow region is usually subject to periarticular problems, including lateral epicondylitis and medial epicondylitis; however, in this chapter, attention is directed to the joint space itself. Aspiration for problems such as synovitis in patients with rheumatoid arthritis and arthrography of the joint for delineation of multiple pathologic processes, including loose bodies, are the initial approaches to treatment.30 When it is determined that an intraarticular injection is needed, the practitioner must remember that the extensor surfaces of the joint are the safest places to avoid vessels and nerves. Thus, the injection should be directed to the posterolateral portion of the elbow or to the posterior portion of the elbow (Figs. 9-6 and 9-7). These approaches will allow the practitioner to enter the humeroulnar joint, the true elbow joint. The patient is placed with the elbow positioned between 50 and 90 degrees of flexion. The posterior and/or lateral skin surfaces are prepared aseptically. For the posterolateral approach, the lateral epicondyle area and the posterior olecranon area are palpated. The groove between the olecranon below and the lateral epicondyle of the humerus is located. The needle is then directed proximally toward the head of the radius and medially into the elbow joint. Again, no resistance should be felt when the needle enters the joint. Aspiration or injection of the joint may then be undertaken. The posterior approach to the elbow is relatively simple. The posterior olecranon is palpated with the lateral olecranon groove located just posterior to the lateral epicondyle. The needle is then inserted above the superior aspect of and lateral to the olecranon. It is advanced into the joint, and, again, no resistance should be felt.

Clavicle Acromion

Sternum

A

Humerus

B

Figure 9-5  Sternoclavicular joint injection technique (A) and surface landmarks (B).

9

68  Soft Tissue and Joint Injections

Humerus

Radius

Ulna

B

A

C

Figure 9-6  Drawing depicting elbow joint injections (A) and surface anatomy (B) lateral, and (C) posterior.

C

R

F

Figure 9-7  Sagittal ultrasound view of the elbow joint. C, Capitellum; R, Radial head; F, Fat pad; Arrowheads, Articular cartilage. (From Jacobson, J, Fundamentals of Musculoskeletal Ultrasound, Philadelphia, Saunders, 2007, p 110.)

Wrist Many of the small joints of the wrist have interconnecting synovial spaces, making it possible to provide relief to the entire joint complex with one injection. The wrist may be infiltrated by several methods.31-33 The route of entry may be influenced by the site of inflammation or desired anatomic area. The preferred method is the dorsal approach, which may be facilitated with slight flexion of the hand. This can be easily accomplished by flexing the hand over a rolled towel. The point of entry (Fig. 9-8) is just medial to the extensor pollicis longus tendon in the distal aspect of the midpoint of the radius and ulna. This can be easily palpated as a depression between the radius and the scaphoid and lunate bones. The needle is placed perpendicular to the skin and inserted 1 to 2 cm lateral to the extensor pollicis longus tendon.32 Optional approaches to the wrist include the ulnar or the dorsal snuffbox approach. With the ulnar approach, the injection is made just distal to the lateral ulnar margin in a palpable gap between the border of the distal ulna and the carpal bones. A third approach is the dorsal aspect just medial

Figure 9-8  Wrist joint injection—dorsal approach. The needle is inserted medial to the extensor pollicis longus tendon.

to the anatomic snuffbox between the radius and carpal bones (Fig. 9-9). Anesthetic and corticosteroid preparations may diffuse throughout the joint and are facilitated by range-of-motion exercises following injection.7,34 The approach used should be based on the area of maximal point tenderness or site of inflammation and specific anatomic structures underlying the region to be infiltrated, such as the scapholunate ligaments or the triangular fibrocartilaginous complex. Caution should be taken to arrive at an accurate diagnosis when treating a chronic condition. An underlying wrist injury with unremarkable initial radiographs may cause scapholunate dissociation, carpal instability, or avascular necrosis. These disorders should be considered in the differential diagnosis during conservative management.

Upper Extremity Joint Injections  69

9

Figure 9-10  Needle placement into the carpometacarpal joint. Figure 9-9  Needle placement adjacent to the anatomic snuffbox between the radius and carpal bones.

Intercarpal Joints Injection into the intercarpal joints such as the triquetrolunate space can be accomplished by palpating the borders of the carpal bone. Palpation is easier to perform when the joint is swollen and fluctuant.33 Ultrasound or fluoroscopic guidance may be necessary for precise location.

Carpometacarpal Joint The first carpometacarpal joint or trapeziometacarpal joint is a frequent source of pain in osteoarthritis and from occupations or sports that subject the patient to undue stress. The joint may be infiltrated or aspirated from the dorsal aspect of the radial side of the carpometacarpal joint (Fig. 9-10) by holding the thumb in slight flexion and palpating for the point of maximal tenderness.14,31,35 When injecting the carpometacarpal joint, care should be taken to avoid the radial artery and the extensor pollicis tendon.36 To avoid the radial artery, the needle should be placed toward the dorsal side of the extensor pollicis brevis tendon.

Interphalangeal Joints The proximal and distal interphalangeal joints are affected most frequently by arthritic processes. The proximal interphalangeal joint is frequently affected in rheumatoid arthritis.12,33 These smaller joints require a small-gauge needle (25- or 27-gauge) to facilitate entry. A vapo-coolant spray may be used for superficial skin anesthesia with or without a superficial skin wheal to diminish the pain on initial infiltration; infiltration of these smaller joints is painful.31 Because the joint space is very small, the tip of the needle must be advanced gently into the intraarticular capsule. The joint will accommodate only a small amount of fluid, usually less than 2 mL, and overdistention should be avoided. Pericapsular and subcutaneous injections have been known to provide some beneficial effect when direct joint infiltration could not be obtained, presumably by transport of the corticosteroids to inflamed capsule and synovium.36 The proximal and distal interphalangeal joints are infiltrated by palpating the borders of the joint and advancing a fine needle, preferably with a small

syringe (2 mL) to facilitate fine motor control. Splinting the affected joint may allow resolution of an inflammatory response.37-39

Conclusion The upper extremity peripheral joints are not difficult to inject. With practice, the clinician can become adept at entering these joints with ease, providing an effective addition to the management of peripheral joint problems. After the joints are injected, they should not be subjected to intensive exercise or motion for several days. This period of relative rest helps to promote the retention of the corticosteroid in the joint, allowing longer contact with the joint surface and delaying absorption of the drug systemically.7 ACKNOWLEDGMENT The editor would like to extend a special thanks to John P. Obermiller, MD and Dennis M. Lox, MD for their original work on this chapter.

REFERENCES   1. Bloom BJ, Alario AJ, Miller LC. Intra-articular corticosteroid therapy for juvenile idiopathic arthritis: Report of an experiential cohort and literature review. Rheumatol Int. 2010 Feb 14.   2. Gray RG, Gottlieb NL. Intra-articular corticosteroids: An updated assessment. Clin Orthop Relat Res. 1983;177:235-263.   3. Bain LS, Balch HW, Wetherly JM, et al. Intra-articular triamcinolone hexacetonide: Double-blind comparison with methylprednisolone. Br J Clin Pract. 1972;26:559-561.   4. Gordon GV, Schumacher HR. Electron microscopic study for depot corticosteroid crystals with clinical studies after intra-articular injection. J Rheumatol. 1979;6:7-14.   5. Perrot S, Laroche F, Poncet C, et al. Are joint and soft tissue injections painful? Results of a national French cross-sectional study of procedural pain in rheumatological practice. BMC Musculoskelet Disord. 2010;11:16.   6. Gowans J, Granieri P. Septic arthritis: Its relation to intra-articular injections of hydrocortisone acetate. N Engl J Med. 1959;261:502-504.   7. Neustadt DH. Local corticosteroid injection therapy and soft tissue rheumatic conditions of hand and wrist. Arthritis. 1991;34:923-926.   8. Gray RG, Gottlieb NL. Rheumatic disorders associated with diabetes mellitus: Literature review. Semin Arthritis Rheum. 1976;6:19-34.

70  Soft Tissue and Joint Injections   9. Kothari T, Reyes MP, Brooks N, et al. Pseudomonas cepacia septic arthritis due to intra-articular injections of methylprednisolone. Can Med Assoc J. 1977;116:1230-1235. 10. Rhee YG, Cho NS, Kim BH, Ha JH. Injection-induced pyogenic arthritis of the shoulder joint. J Shoulder Elbow Surg. 2008;17(1):63-67. 11. Stanley D, Conolly WB. Iatrogenic injection injuries of the hand and upper limb. J Hand Surg Br. 1992;17:442-446. 12. Pfenninger JL. Injections of joints and soft tissue: Part I. General guidelines. Am Fam Physician. 1991;44:1196-1202. 13. Stefanich RJ. Intra-articular corticosteroids in treatment of osteoarthritis. Orthop Rev. 1986;15:65-71. 14. Hollander JL. Intrasynovial corticosteroid therapy in arthritis. Md State Med J. 1970;19:62-66. 15. Hardin JG Jr. Controlled study of the long-term effects of “total hand” injection. Arthritis Rheum. 1979;22:619. 16. de Mos M, et al. Can platelet rich plasma enhance tendon repair? A cell culture study. Am J Sports Med. 2008;36(6):1171-1178. 17. Hajjioui A, Nys A, Poiraudeau S, Revel M. An unusual complication of intra-articular injections of corticosteroids: Tachon syndrome. Two case reports. Ann Readapt Med Phys. 2007;50(9):721-723. 18. Hurvitz AP, Hodapp KL, Jadgchew J, et al. Central serous chorioretinopathy resulting in altered vision and color perception after glenohumeral corticosteroid injection. Orthopedics. 2009 Aug;32(8). 19. Noel E, Hardy P, Hagena FW, et al. Efficacy and safety of Hylan G-F20 in shoulder osteoarthritis with an intact rotator cuff. Open-label prospective multicenter study. Joint Bone Spine. 2009 Dec;76(6):670-673. 20. Peterson C, Hodler J. Evidence-based radiology (Part 2): Is there sufficient research to support the use of therapeutic injections into the peripheral joints? Skeletal Radiol. 2010;39(1):11-18. 21. Anitua E, Andía I, Sanchez M, et al. Autologous preparations rich in growth factors promote proliferation and induce VEGF and HGF production by human tendon cells in culture. J Orthop Res. 2005;23: 281-286. 22. Menetrey J, Kasemkijwattana C, Day CS, et al. Growth factors improve muscle healing in vivo. J Bone Joint Surg Br. 2000;82:131-137. 23. Yasuda K, Tomita F, Yamazaki S, et al. The effect of growth factors on biomechancical properties of the bone-patellar tendon-bone graft after anterior cruciate ligament reconstruction: a canine model study. Am J Sports Med. 2004;32:870-880. 24. Mishra A, Pavelko T. Treatment of chronic elbow tendinosis with buffered platelet rich plasma. Am J Sports Med. 34(11):1774-1778. 25. Sanchez M, Azofra J, Anitua E, et al. Plasma rich in growth factors to treat an articular cartilage avulsion: A case report. Med Sci Sports Exerc. 2003;35:1648-1652. 26. Sánchez M, Anitua E, Azofra J, et al. Comparison of surgically repaired Achilles tendon tears using platelet-rich fibrin matrices. Am J Sports Med. 2007;35:245-251. 27. Gray RG, Tenenbaum J, Gottlieb NL. Local corticosteroid injection treatment in rheumatic disorders. Semin Arthritis Rheum. 1981;10:231-254. 28. Doherty M, Hazleman BL, Hutton CW, et al. Rheumatology Examination and Injection Techniques. Philadelphia: WB Saunders; 1992.

29. Jacobs LG, Smith MG, Khan SA, et al. Manipulation or intra-articular steroids in the management of adhesive capsulitis of the shoulder? A prospective randomized trial. J Shoulder Elbow Surg. 2009;18(3): 348-353. 30. Hudson TM. Elbow arthrography. Radiol Clin North Am. 1981; 19:227-241. 31. Leversee JH. Aspiration of joint and soft tissue injections. Prim Care. 1986;13:579-599. 32. Pfenninger JL. Infections of joints and soft tissues: Part II. Guidelines for specific joints. Am Fam Physician. 1991;44:1690-1701. 33. Steinbrocker O, Neustadt DH. Aspiration Injection Therapy in Arthritis and Musculoskeletal Disorders: Handbook on Technique and Management. Hagerstown, Md: Harper & Row; 1972. 34. Owen DF. Intra-articular and soft tissue aspiration injection. Clin ­Rheumatol Pract (Mar-May). 1986:52-63. 35. Wilke WS, Tuggle CJ. Optimal techniques for intra-articular and periarticular joint injections. Mod Med. 1988;56:58-72. 36. Taweepoke P, Frame JD. Acute ischemia of the hand by accidental radial infusion of Depo-Medrone. J Hand Surg Br. 1990;15:118-120. 37. Howard LD, Pratt ER, Punnell S. The use of compound F (hydrocortisone) in operative and nonoperative conditions of the hand. J Bone Joint Surg Am. 1953;35:994-1002. 38. Marks M, Gunther SF. Efficacy of cortisone injection in treatment of trigger fingers and thumbs. J Hand Surg Am. 1989;14:722-727. 39. FaunØ P, Andersen HJ, Simonsen O. A long-term follow up of the effects of repeated corticosteroid injections for stenosing tenovaginitis. J Hand Surg Br. 1989;14B:242-243. 40. Shortt CP, Morrison WB, Roberts CC, et al. Shoulder, hip, and knee arthrography needle placement using fluoroscopic guidance: Practice patterns of musculoskeletal radiologists in North America. Skeletal Radiol. 2009;38(4):377-385. 41. Alarcon-Segovia D, Ward LE. Marked destructive changes occurring in osteoarthritic finger joints after intra-articular injection of corticosteroids. Arthritis Rheum. 1966;9:443-463. 42. Jalava S. Periarticular calcification after intra-articular triamcinolone hexacetonide. Scand J Rheumatol. 1980;9:190-192. 43. Bliddal H, Terslev L, Qvistgaard E, et al. A randomized, controlled study of a single intra-articular injection of etanercept or glucocorticosteroids in patients with rheumatoid arthritis. Scand J Rheumatol. 2006; 35(5):341-345. 44. McCarty DJ, McCarthy G, Carrera G. Intra-articular corticosteroids possibly leading to local osteonecrosis and marrow fat-induced synovitis. J Rheumatol. 1991;18:1091-1094. 45. Castles JJ. Clinical pharmacology of glucocorticoids. In: McCarty DJ, Hollander JL, eds. Arthritis and Allied Conditions. 12ed. Philadelphia: Lea & Febiger; 1993:665-682. 46. Behrens F, Shepard N, Mitchell N. Alterations of rabbit articular cartilage by intra-articular injection of glucocorticoids. J Bone Joint Surg Am. 1975;57A:70-76. 47. Zuckerman JD, Meislin RJ, Rothberg M. Injections for joint and soft tissue disorders: When and how to use them. Geriatrics. 1990;4:45-52.

10

Lower Extremity Joint ­Injections Ted A. Lennard, MD

Lower extremity intraarticular injections with corticosteroids and anesthetics are useful treatment options for patients with hip, knee, ankle, or foot pain.4 Injections are given to treat acutely painful joints refractory to rest and oral medications. The indications, patient selection, complications,1,2,6,7,9,14,16,19 and general technique of joint injections10,25 were covered in the previous chapter. This chapter will focus on the technique of specific lower extremity intraarticular joint injections. Knowledge of multiple techniques is helpful.26

Hip Joint The hip joint is often difficult to infiltrate or aspirate because of its depth and the surrounding tissue. Fluoroscopic guidance with injection of contrast material or ultrasound guidance is often necessary to confirm proper needle placement. This joint may be infiltrated by an anterior or lateral approach (Figs. 10-1, 10-2, 10-3). The anterior approach is preferred.18,23,24 With the anterior approach, the patient is in the supine position with the lower extremity externally rotated. The length of the needle will depend on the patient’s size. The anatomic landmarks for the anterior approach are 2 cm distal to the anterior superior iliac spine and 3 cm lateral to the palpated femoral artery at a level corresponding to the superior margins of the greater trochanter. After superficial anesthesia is administered, the needle is advanced at an angle 60 degrees posteromedially through the tough capsular ligaments, advanced to bone, and slightly withdrawn. This technique places the tip of the needle directly into the joint, and aspiration or injection may be performed. This approach is much simpler using image guidance to direct the needle posteromedially into the joint. When the capsular ligaments have been penetrated, 2 to 4 mL of anesthetic and corticosteroid suspension may be introduced. The lateral approach is performed by palpating the greater trochanter of the femur, which may be facilitated by externally rotating the lower extremity. Superficial anesthesia may be used and, again, depending on the size of the patient, the appropriate-length needle is selected. A 3- to 4-inch needle is usually sufficient; however, in larger patients, longer needles may be necessary. Just anterior to the greater trochanter, the needle is advanced and walked medially along the neck of the femur until the joint is reached. Aspiration may be obtained but is more difficult with the lateral approach. The amount of fluid that may be introduced may be limited, depending on the integrity of the joint.

Knee The knee is the most commonly aspirated and injected joint in the body. It contains the largest synovial space and demonstrates the most visible and palpable effusion (when present). A patient is usually most comfortable lying supine with sufficient pillows. The knee is prepared using an aseptic technique. If a large effusion is present, whether medially or laterally, the site of entry should be over the maximal expansion of the effusion in order to cause the least discomfort during the procedure. For injections in which a large effusion is not present, the lateral, medial, suprapatellar, or anterior approach may be used (Fig. 10-4). Before injecting or aspirating the knee, the patella should be grasped between the examiner’s thumb and forefinger and rocked gently from side to side to ensure that the patient’s muscles are relaxed. The medial approach to the knee is simple. First, the practitioner puts a small amount of lateral pressure on the patella, pushing it slightly medially and displacing it somewhat to increase the gap between the patella and the femur medially. The needle is then introduced about midway between the superior and inferior pole of the patella, medial to the patella and midway between the medial border of the patella and the femur. A preinjection skin wheal may be raised with an anesthetic agent, or the skin itself may be anesthetized with a vapo-coolant spray for patient comfort. As the needle is introduced into the joint space, the needle should be aspirated progressively. If no aspirate is obtained, the corticosteroid can be injected. Before withdrawal of the needle, the needle tract again should be flushed with a small amount of anesthetic. The lateral approach to the knee is also simple. With the patient supine, the knee is fully extended or placed in slight flexion. The patella is slightly displaced laterally to increase the gap between the patella and femur laterally. The skin may then be anesthetized with 1% lidocaine. The needle is introduced halfway between the superior pole of the patella and the midline of the patella lateral and inferior to the patella. As the needle is introduced, aspiration is performed until the needle is inside the joint. The joint can then be aspirated or injected. If a large effusion is present, the suprapatellar approach may be used. This does not have any specific advantage over the lateral approach unless the effusion is expanding the suprapatellar bursa. The needle is introduced at the point of maximal expansion of the effusion, and the joint is then aspirated. This approach is usually not as good as the lateral approach if the knee is to be injected only 71

72  Soft Tissue and Joint Injections

I

A

H N

Figure 10-1  Intraarticular injection of the hip joint, lateral approach.

A

Femoral nerve Femoral artery Femoral vein I

H

B

Figure 10-2  Intraarticular injection of the hip joint, anterior approach.

and not aspirated. It is much easier to enter the joint space with the medial or lateral approach. On occasion, an anterior approach to the knee may be desired if a patient cannot fully extend the knee. In these cases, the patient may be sitting or supine with the knee flexed to 90 degrees. The needle is inserted just inferior to the inferior patellar pole from either the lateral or medial side of the patellar tendon. The needle is then advanced parallel to the tibial plateau until the joint space is entered. It is more difficult to aspirate a knee effusion when using this approach.23 Moreover, the risk of puncturing the articular cartilage is much higher, as is the risk to the infrapatellar fat pad. Occasionally, the knee is approached anteriorly by inserting the needle directly through the patellar tendon. This approach has no merit because it increases discomfort to the patient and may cause bleeding in the patellar ligament.

Figure 10-3  A, Sagittal ultrasound view of the proximal hip joint. B, Transverse ultrasound view of the proximal hip joint. A, Acetabulum; H, Femoral head; I, Iliopsoas muscle; N, Femoral neck. Arrowhead denotes the collapsed anterior joint recess. Arrow denotes the labrum. (From Jacobson J: Fundamentals of Musculoskeletal Ultrasound, WB Saunders, 2007, p 182.)

Ankle Mortise The ankle joint is not commonly injected; however, it may be subject to osteoarthritis, rheumatoid arthritis, or chronic pain resulting from instability.8,12,13,27,28 An anterior medial or anterior lateral approach may be used, depending on the location of pain or pathologic process (Figs. 10-5 and 10-6). For the medial approach, a slight depression is felt between the extensor hallucis longus tendon laterally and tibialis anterior tendon medially on the inferior border of the tibia superiorly and the talus inferiorly. The needle is then directed slightly laterally and perpendicular to the tibial joint surface. The talus has a superior curve, and the needle may need to be angled slightly superiorly to avoid contact with the talar joint surface.

Lower Extremity Joint Injections  73

10

Femur

Patella

Tibia

Fibula

A

C

B

Figure 10-4  A, Drawing of medial and lateral injection approaches to the knee. Surface location of a lateral (B) and medial (C) injection.

Fibula

Tibia Talus

Calcaneus

A

C

B

D

Figure 10-5  A, Drawing of the different approaches to an ankle injection. Surface location of a medial (B), lateral (C), and posterior (D) sites for injections.

The lateral approach is useful in situations in which pathologic processes in the ankle appear to be most prominent either at the talofibular joint or the tibiotalar joint. Here, the foot is placed in moderate plantar flexion. The area enclosed by the tibia superiorly, the talus inferiorly, and the fibular head laterally is palpated. The

extensor tendons of the toes should be medial to the injection site. The needle is then inserted from an anterolateral position and is directed toward the posterior edge of the medial malleolus. If the joint surface is encountered, the physician should direct the needle slightly upward, remembering that the talar dome arches superiorly.

74  Soft Tissue and Joint Injections

Tib

F Tal

Figure 10-6  Ultrasound image of the ankle joint. Sagittal imaging reveals the anterior fad pad (F), between the tibia (Tib) and talus (Tal). Arrowheads depict the hyaline articular cartilage. (From Jacobson J: Fundamentals of Musculoskeletal Ultrasound, WB Saunders, 2007, p 272.)

Figure 10-7  Dorsal approach to the first metatarsophalangeal joint.

Conclusion Subtalar Joint Occasionally, the subtalar joint is the site of a pathologic process.3 The easiest approach to this joint is to have the patient lie prone with his or her feet extending over the end of the examination table. This allows the ankle to be in the neutral position. The posterior and lateral portions of the ankle are then prepared aseptically. The site of entry for the injection is along a line drawn from the most prominent portion of the distal fibula posterior to the Achilles tendon. This line should be parallel to the plantar aspect of the foot with the foot in neutral position; halfway between the prominent aspect of the lateral malleolus and the Achilles tendon, the needle is inserted and directed toward a point inferior and medial to the medial malleolus. Fluoroscopic or ultrasound guidance can be very helpful during subtalar joint injections.5.11,15,17

Intertarsal Joints Injection of the tarsal joints may be accomplished similarly to injection of the carpal joints. Palpation of the bony landmarks is carried out, the needle is inserted between the tarsal bones to the desired depth, and aspiration is accomplished if necessary. Fluoroscopic needle guidance simplifies this procedure and ascertains precise needle placement.

Metatarsophalangeal Joints The metatarsophalangeal joints are most frequently infiltrated with a dorsal approach (Fig. 10-7). This approach is carried out by palpating the metatarsophalangeal margins with plantar flexion of the toe to facilitate insertion of the needle. The needle is then advanced into the joint. The first metatarsophalangeal joint is frequently affected by arthritic conditions and gout. When a swollen joint is encountered, infiltration and aspiration may be easier with a swollen capsule.

The lower extremity peripheral joints are not difficult to inject. With the use of ultrasound or fluoroscopic guidance, the clinician can become adept at entering these joints with ease, providing an effective addition to the management of peripheral joint problems. ACKNOWLEDGMENT The editor would like to extend a special thanks to John P. Obermiller, MD and Dennis M. Lox, MD for their original work on this chapter. REFERENCES   1. Bliddal H, Qvistgaard E, Terslev L, et al. A randomized, controlled study of a single intra-articular injection of etanercept or glucocorticosteroids in patients with rheumatoid arthritis. Scand J Rheumatol. 2006; 35(5):341-345.   2. Hajjioui A, Nys A, Poiraudeau S, Revel M. An unusual complication of intra-articular injections of corticosteroids: Tachon syndrome. Two case reports. Ann Readapt Med Phys. 2007;50(9):721-723.   3. Shortt CP, Morrison WB, Roberts CC, et al. Shoulder, hip, and knee arthrography needle placement using fluoroscopic guidance: Practice patterns of musculoskeletal radiologists in North America. Skeletal Radiol. 2009;38(4):377-385.   4. Pfenninger JL. Infections of joints and soft tissue: Part I. General guidelines. Am Fam Physician. 1991;44:1196-1202.   5. Beukelman T, Arabshahi B, Cahill AM, et al. Benefit of intraarticular corticosteroid injection under fluoroscopic guidance for subtalar arthritis in juvenile idiopathic arthritis. J Rheumatol. 2006;33(11):2330-2336.   6. Cahill AM, Cho SS, Baskin KM, et al. Benefit of fluoroscopically guided intraarticular, long-acting corticosteroid injection for subtalar arthritis in juvenile idiopathic arthritis. Pediatr Radiol. 2007;37(6):544-548.   7. Henning T, Finnoff JT, Smith J. Sonographically guided posterior subtalar joint injections; Anatomic study and validation of 3 approaches. PM R. 2009;1(10):925-931.   8. Khosla S, Thiele R, Baumhauer JF. Ultrasound guidance for intra-articular injections of the foot and ankle. Foot Ankle Int. 2009;30(9):886-890.   9. Kirk KL, Campbell JT, Guyton GP, Schon LC. Accuracy of posterior subtalar joint injection without fluoroscopy. Clin Orthop Relat Res. 2008;466(11):2856-2860. 10. Hasegawa M, Nakoshi Y, Tsujii M, et al. Changes in biochemical markers and prediction of effectiveness of intra-articular hyaluronan in patients with knee osteoarthritis. Osteoarthritis Cartilage. 2008;16(4):526-529.

Lower Extremity Joint Injections  75 11. Gray RG, Gottlieb NL. Rheumatic disorders associated with diabetes mellitus: Literature review. Semin Arthritis Rheum. 1976;6:19-34. 12. Hollander JL. Intrasynovial corticosteroid therapy in arthritis. Md State Med J. 1970;19:62-66. 13. Hollander JL. Joint problems in the elderly: How to help patients cope. Postgrad Med. 1988;84:209-211,215-216. 14. Jalava S. Periarticular calcification after intra-articular triamcinolone hexacetonide. Scand J Rheumatol. 1980;9:190-192. 15. Gray RG, Tenenbaum J, Gottlieb NL. Local corticosteroid injection treatment in rheumatic disorders. Semin Arthritis Rheum. 1981;10:231-245. 16. Kothari T, Reyes MP, Brooks N, et al. Pseudomonas cepacia septic arthritis due to intra-articular injections of methylprednisolone. Can Med Assoc J. 1977;116:1230-1235. 17. Balch HW, Gibson JM, El-Ghobarey AF, et al. Repeated corticosteroid injections into knee joints. Rheumatol Rehabil. 1977;16:137-140. 18. Leversee JH. Aspiration of joint and soft tissue injections. Prim Care. 1986;13:579-599. 19. McCarty DJ, McCarthy G, Carrera G. Intra-articular corticosteroids possibly leading to local osteonecrosis and marrow fat-induced synovitis. J Rheumatol. 1991;18:1091-1094. 20. Owen DF. Intra-articular and soft tissue aspiration injection. Clin ­Rheumatol Pract (Mar-May). 1986:52-63.

21. Peterson C, Hodler J. Evidence-based radiology (Part 2): Is there sufficient research to support the use of therapeutic injections into the peripheral joints? Skeletal Radiol. 2010;39(1):11-18. 22. Perrot S, Laroche F, Poncet C, et al. Are joint and soft tissue injections painful? Results of a national French cross-sectional study of procedural pain in rheumatological practice. BMC Musculoskelet Disord. 2010;11(1):16. 23. Adleberg JS, Smith GH. Corticosteroid-induced avascular necrosis of the talus. J Foot Surg. 1991;30:66-69. 24. Pfenninger JL. Injections of joints and soft tissues: Part II. Guidelines for specific joints. Am Fam Physician. 1991;44:1690-1701. 25. Shimizu M, Higuchi H, Takagishi K, et al. Clinical and biochemical characteristics after intra-articular injection for the treatment of osteoarthritis of the knee: Prospective randomized study of sodium hyaluronate and corticosteroid. J Orthop Sci. 2010;15(1):51-56. 26. Gordon GV, Schumacher HR. Electron microscopic study for depot corticosteroid crystals with clinical studies after intra-articular injection. J Rheumatol. 1979;6:7-14. 27. Stefanich RJ. Intra-articular corticosteroids in treatment of osteoarthritis. Orthop Rev. 1986;15:65-71. 28. Wilke WS, Tuggle CJ. Optimal techniques for intra-articular and periarticular joint injections. Mod Med. 1988;56:58-72.

10

Bursae Injections

11

Nicholas K. Olsen, DO, Joel M. Press, MD, and ­Jeffrey L. Young, MD Bursitis is commonly diagnosed and treated in clinical practices that focus on musculoskeletal medicine. Inflamed bursae often respond to conservative treatments including rest, cryotherapy, compression, physical/occupational therapy and nonsteroidal antiinflammatory drugs (NSAIDs).1a In patients who fail to respond to conservative rehabilitation, a corticosteroid injection into the bursa can serve as a useful diagnostic and therapeutic adjunct to a comprehensive course of rehabilitation. Bursae are purse-like sacs containing fluid and function to reduce friction at a joint. They are positioned between two muscles or between a muscle and its tendon or bone. Inflammation may occur during repetitive activities involving poor body mechanics or following direct trauma. An accurate diagnosis includes a thorough history, and an investigation of the occupational and recreational factors predisposing a patient to repetitive overload or joint stress. Correction of improper biomechanics is essential to reduce joint tension early in the course of treatment to avoid chronic bursitis. Physical examination will reveal focal tenderness, swelling, and pain during direct palpation. If the injury is due to acute trauma, a fracture or ligamentous instability of the joint should be considered. In cases of chronic bursitis, calcifications may be identified on plain radiographs. However, the most common etiology combines repetitive motion with improper biomechanics. The physical examination should include a survey of peripheral joints to rule out a systemic process such as an underlying rheumatic disease. Skin overlying the area of tenderness should be examined for evidence of warmth, redness, swelling, or penetrating trauma. Rarely an infected bursa is diagnosed, and skin warmth appreciated on palpation may be the most sensitive physical indicator.1 The treatment of bursitis requires that an infection be considered prior to initiating treatment protocols. Aspiration of a septic bursa and identification of a bacterial pathogen are necessary to initiate appropriate antibiotic treatment. Laboratory studies of the serum should include an erythrocyte sedimentation rate, complete blood cell count, and microscopic examination to screen for leukocytosis, bacteria on Gram stain, or crystals. Operative incision and drainage of a septic bursa may be required for effective treatment.2,3 Con­ traindications to bursal injection with corticosteroids include cellulitis, generalized infection, and coagulation disorders. Bursal injections serve a diagnostic and a therapeutic role. An initial bursal injection with local anesthetic alone can provide important information that will confirm the diagnosis. Bursitis from a noninfectious etiology may be considered for an injection of corticosteroid and anesthetic reducing bursal pain and inflammation, thereby allowing the patient to engage in a comprehensive

rehabilitation program. Following the injection, the patient should be given instructions to ice and observe relative rest prior to resumption of a therapeutic exercise program. The clinician should direct the patient in a home exercise program and a physical therapist may be consulted for soft tissue mobilization and instruction in a stretching and strengthening program. Ice may be a useful adjunct during the initial phases of treatment, and NSAIDs may provide additional relief. Each of these options should be individualized for the clinical situation, and none of these, especially bursal injections, is to be used as the primary form of therapy. Re-examination should be scheduled within the first few weeks, and the rehabilitative program should be tailored to the patient as symptoms subside. This chapter describes the basic approach to injection of many of the bursae encountered in clinical practice. Although the rehabilitation program for each bursa has not been detailed to allow for closer attention to procedural techniques, it is essential to employ a comprehensive rehabilitation to maximize the success of injections.

Subacromial (Subdeltoid) Bursitis The subacromial bursa rests on the supraspinatus and is covered by the acromion, the coracoacromial ligament, and the deltoid. This is the most common site of bursitis of the shoulder, with inflammation usually occurring secondary to rotator cuff tendinitis or shoulder impingement syndrome. In a pure subacromial bursitis, the impingement signs may be absent, and the inflamed bursa may limit full passive abduction due to compression at the near end range of shoulder motion.4 More commonly, subacromial bursitis coexists with impingement syndrome or rotator cuff syndrome. Determining the etiology of shoulder pain may be difficult, and a diagnostic injection into the bursa can narrow the field of possibilities. A diagnostic injection may help distinguish weakness and loss of range of motion secondary to a painful bursitis from a full-thickness rotator cuff tear. The patient should be thoroughly examined prior to the administration of local anesthetic and then reexamined 5 to 10 minutes after injection. Postinjection, the patient may be less guarded and more cooperative during the physical examination, yielding further diagnostic information. Although an anterior, posterior, or lateral approach may be used, the posterolateral approach is preferred. Following sterile technique, the skin is cleansed with povidone-iodine, and the patient is directed to retract the shoulder to a neutral posture. The posterolateral angle of the acromion is identified by palpation, and the needle is advanced in an anteromedial and slightly inferior 77

78  Soft Tissue and Joint Injections

direction (Figs. 11-1 and 11-2).5 If the soft tissues resist needle insertion, a small volume can be injected to expand the bursa so that the needle can be advanced further, resulting in optimal needle position. A mixture of 2 to 4 mL of 1% or 2% lidocaine hydrochloride and 2 to 4 mL of 0.5% bupivacaine hydrochloride is injected into the bursa after a 25-gauge, 1.5-inch needle is introduced approximately 1 inch.6 In the authors’ experience, an inflamed subacromial bursa accepts 4 to 6 mL of total volume. Following the injection, a reduction of pain with improved strength supports the diagnoses of shoulder impingement, supraspinatus tendinitis, and subdeltoid bursitis. Patients who respond with greater than 50% relief are good candidates for an immediate follow-up injection with 1 mL of betamethasone sodium phosphate.6 Alternatively, the anesthetics can be mixed with the corticosteroids and administered in a single injection when the clinical examination is clear. Subacromial bursography is helpful when the initial blind anesthetic injection is unsuccessful or in a patient whose diagnosis is unclear.

A normal bursogram casts doubt on a diagnosis of subacromial impingement.7 The strengthening component of a rehabilitative program should not progress too rapidly after corticosteroid injection, to avoid aggravation of inflammation and to avoid the rare risk for tendon rupture.

Olecranon Bursitis (Draftsmen’s Elbow) The olecranon bursa is subcutaneous, protecting the proximal ulna frequently subjected to trauma. Inflammation of this bursa is commonly associated with rheumatologic disorders. Aspiration of the bursa should always precede injection and may be helpful to ensure proper location of the needle because the wall of the bursa is often thickened and fibrotic from chronic irritation. Gout may be seen at the olecranon, and any bursal fluid aspirated should undergo microscopic examination for crystals. Aspiration of the bursa is more successful using a larger bore needle (18 gauge), because the fluid may be gelatinous. The needle enters the skin perpendicular to the central swelling while the clinician withdraws on the syringe (Fig. 11-3).5 The procedure is followed with the application of a compressive dressing, and the patient is instructed to protect the elbow from further trauma. Persistent cases may benefit from a low-dose corticosteroid injection. Rarely, surgical excision or an arthroscopic bursectomy is warranted after failure of conservative measures.2

Trochanteric Bursitis

Figure 11-1  The subacromial bursa is approached from posterolateral attitude.

Several bursae may be implicated in trochanteric bursitis. The subgluteus maximus bursa lies lateral to the greater trochanter and the insertion of the gluteus medius and minimus. The subgluteus medius bursa is situated superior and posterior to the trochanter. The gluteus minimus bursa lies anterior to the trochanter. All three bursae may be part of a greater trochanteric pain syndrome. Trochanteric bursitis is commonly seen in an elderly population and manifests as pain in the lateral thigh during ambulation.5a Patients may describe a pseudoradicular pattern with the pain extending down the lateral aspect of the lower extremity and into

Coracoid Humeral head Radial head

Lateral epicondyle

Olecranon

Figure 11-2  Schematic of subacromial bursa injection. (Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)

Figure 11-3  Approach for olecranon aspiration and injection. (Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)

Bursae Injections  79

the buttock. The symptoms can be elicited by placing the lower extremity in external rotation and abduction. Direct palpation or deep pressure applied posterior and superior to the trochanter will reproduce the pain.8 The patient should be examined for limita­ tions in flexibility involving the gluteus maximus, medius, and minimus and the tensor fasciae latae. Trendelenburg gait as a result of hip abduction weakness may contribute to increased friction and irritation of the bursa. If the history and physical examination are consistent with bursitis, a corticosteroid combined with anesthetic agent is delivered via a 3.5-inch, 22-gauge needle directed at the point of maximal tenderness overlying the greater trochanter (Fig. 11-4).5,9 Persistent hip pain despite injection therapy and comprehensive rehabilitation should alert the physician to alternate sources of pain including the lumbar spine, hip joint, and distal lower extremity joints.10,11

Iliopectineal Bursa The iliopectineal (iliopsoas) bursa, the largest bursa near the hip joint, is located anterior to the hip capsule and is covered by the iliopsoas. Inflammation of the bursa is not particularly common and may be functionally limiting in that it causes the patient to avoid extension of the lower extremity during the gait cycle. Patients hold the lower extremity in external rotation with the hip in flexion to relieve pressure on the inflamed bursa. Referral pain following the femoral nerve distribution may be seen in cases of iliopectineal bursitis. The examiner may elicit symptoms by passively extending the hip in either a supine or prone position. Injection under fluoroscopic guidance is recommended because the bursa may communicate with the hip capsule and correct needle placement is essential.8,12 Once placement is confirmed by a bursogram, a mixture of anesthetic and corticosteroid is injected through the 3.5-inch spinal needle.

Ischial Bursitis The ischial bursa lies between the ischial tuberosity and the gluteus maximus. The examiner’s index of suspicion must be high because ischial bursitis—so-called “tailor’s or weaver’s bottom”—is not common. Classically, ischial bursitis occurs from friction and the

trauma of prolonged sitting on a hard surface. It may occur in adolescent runners, often in conjunction with ischial apophysitis. Pain is most commonly aggravated during uphill running.13 The pain is distributed down the posterior aspect of the thigh and occurs with activation of the hamstring muscles. Initial treatment approaches should address modification of the patient’s activity, including a decrease in the duration and frequency of running. If an alternative to running includes cycling, the patient should be advised to avoid the use of toe clips, which increase activation of the hamstrings. When the etiology is due to prolonged sitting, the patient’s work station should be modified to allow activities to be conducted in a standing position, and a cushion should be used during sitting. Ice and NSAIDs are helpful in controlling symptoms. Adolescent athletes may require a radiologic series to screen for callus formation secondary to ischial apophysitis if the pain does not resolve with conservative measures. Persistent pain may benefit from injection as an adjunct to rest, ice, and NSAIDs. To perform this, the patient lies on his or her side with the knees fully flexed to relax the hamstrings. A 3-inch, 22-gauge needle is held in a horizontal position and directed toward the point of maximal tenderness overlying the ischial tuberosity. The injection of contrast dye into the bursa under fluoroscopy may be necessary to verify needle placement.

Anserine Bursitis The anserine bursa separates the three conjoined tendons of the pes anserinus, or goose’s foot (semitendinosus, sartorius, and gracilis muscles), from the medial collateral ligament and the tibia. It is one of the most commonly inflamed bursae in the lower extremity. Anserine bursitis is commonly seen in women with heavy thighs and osteoarthritis of the knees. The bursa may also become inflamed as the result of direct trauma in athletes, especially soccer players.4,13 Patients report pain inferior to the anteromedial surface of the knee with ascension of stairs. Moving the patient’s knee in flexion and extension while internally rotating the leg will reproduce the symptoms. The palpatory examination will localize the pain to the anserine bursa. The injection is straightforward and effective in reducing inflammatory symptoms. After sterile preparation, the knee is fully extended and a 1.0- to 1.5-inch, 22-gauge needle is directed at the point of maximal tenderness (Fig. 11-5)5 to deliver a 1- to 3-mL

Patella

Femur

Tibia

Pes anserine bursa Greater trochanteric bursa Figure 11-4  Greater trochanteric bursal injection. (Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)

Figure 11-5  Anserine bursal injection. (Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)

11

80  Soft Tissue and Joint Injections

combination of anesthetic and corticosteroid. The patient should enter a rehabilitation program emphasizing flexibility, and the athlete at risk for repetitive trauma may benefit from padded knee protection.

Tibial Collateral Ligament Bursitis The tibial collateral ligament (TCL) bursa, referred to as the “no name, no fame” bursa,14 is located between the deep and superficial aspects of the tibial collateral ligament.14a The bursa does not adhere to the medial meniscus, and it appears to reduce friction between the superficial layer of the TCL and the medial meniscus. TCL bursitis should be considered in any patient with medial joint line tenderness. During a 3-year study, Kerlan found that 5% of orthopedic patients presenting with medial knee pain suffered from TCL bursitis.15 Physical examination will not show evidence of new ligamentous or capsular instability. Treatment consists of a local injection of lidocaine (2 to 4 mL) and 1 mL of triamcinolone (40 mg/mL)15 directed perpendicular to the medial joint line at the point of maximal tenderness (Fig. 11-6).

Prepatellar Bursitis Prepatellar bursitis, often called “housemaid’s knee,” is the result of frequent kneeling that produces swelling and effusion of the subcutaneous bursa at the anterior surface of the patella. The patient infrequently complains of pain unless direct pressure is applied to the bursa. The area is easily entered with a needle at the middle to superior pole of the patella. Repeat injections may be required because the bursa is often multiloculated. Occupational adjustments should include patient education, avoidance of kneeling, and the use of knee pads when pressure must be applied to the patella. A Cryo/cuff can be used to control the inflammatory response in a bursitis that approximates a peripheral joint.

Infrapatellar Bursitis Infrapatellar bursitis, or clergyman’s knee, occurs with pressure from direct kneeling. The bursa rest on the superior anterior pole of the tibia and is covered by the infrapatellar tendon. Rest and avoidance of direct pressure, cryotherapy with compression and

improved flexibility in the quadriceps mechanism are advised. The rehabilitation effort should be maximized prior to consideration of injection therapy because the tendon is at risk for ruptures with administration of corticosteroids.

Retrocalcaneal (Subtendinous) Bursitis The retrocalcaneal bursa lies between the posterior surface of the calcaneus and the tendon of the triceps surae. Inflammation of the bursa may occur from overtraining, such as too early assumption of increased mileage in a runner, or an ill-fitting shoe resulting in pressure from a restricting heel counter. A positive indicator is discomfort when the examiner places the thumb and index finger on the anterior edges of the Achilles tendon and applies pressure. Modification of the footwear is an important first step to alleviating pain, and symptoms should be controlled with ice and NSAIDs. As the pain is controlled, the patient should stretch the triceps surae complex daily to avoid recurrence. Injections into the bursa are considered only after the aforementioned measures have been pursued. A 20- to 22-gauge needle should be inserted where the bursa demonstrates the greatest distention, often on the lateral aspect of the heel. The needle is advanced with an anterior angle of 15 to 20 degrees to avoid instilling corticosteroid into the Achilles tendon, which weakens the structure and increases the risk of tendon rupture.

Subcutaneous Bursitis Subcutaneous bursitis, also known as Achilles bursitis or achillobursitis, affects the bursa that lies subcutaneous to the posterior surface of the tendon. Midline swelling develops where the upper edge of the heel counter comes in contact with the heel cord. Subcutaneous bursitis is common in patients who wear high-heeled shoes that apply direct pressure on the bursa. The mainstay of treatment is to have the patient change the shoes. Ice and antiinflammatory medications help provide symptomatic relief. Injection of the bursa is usually not necessary, but if the symptoms persist, an injection may be considered. Care should be given to avoid the Achilles tendon because it is susceptible to rupture.

Calcaneal Bursitis Calcaneal bursitis often develops in elderly patients from a calcified spur that subjects the bursa to trauma after prolonged walking or running. Evaluation of the footwear may reveal poor shock-absorbing capacity. Injection into the point of maximum tenderness may have diagnostic and therapeutic value. Selection of an appropriate walking or running shoe and the use of a heel cup are beneficial. Athletes should be encouraged to change running shoes every 200 to 300 miles because midsole breakdown occurs after this amount of wear.16

Pharmacologic Agents for Bursal Injection

Figure 11-6  Approach for tibial collateral bursa.

A number of local anesthetics are available for bursal injections, and clinicians should be familiar with their pharmacologic properties. Concentrations of 0.5% to 1.0% lidocaine or 0.25% to 0.5% bupivacaine are appropriate for bursal injection. The onset and

Bursae Injections  81

duration of the anesthetic effect is related to the volume and concentration injected. Lidocaine has an onset of action within 5 to 15 minutes and may last 3 to 4 hours, whereas bupivacaine begins to work in 10 to 20 minutes, but the anesthetic effect can last 4 to 6 hours.17 Bach describes the benefits of using a combination of lidocaine hydrochloride and bupivacaine hydrochloride in subacromial space injections to obtain an early onset of action with prolonged anesthesia.6 Corticosteroids are widely available and very effective in alleviating bursal inflammation. Corticosteroids of intermediate or long duration are suitable for treatment of bursitis. Triamcinolone acetonide (10 mg/mL and 40 mg/mL) is a commonly used intermediate-acting agent with a half-life of 24 to 36 hours. Betamethasone is a longer acting corticosteroid with a half-life of 36 to 72 hours and a relative antiinflammatory potency five times greater than triamcinolone.17 The dosage is adjusted to the size of the bursa, and the lowest effective dose should be delivered to the bursa. Clinicians may want to avoid corticosteroid injection acutely (the first 7 days after an initial injury) because corticosteroids theoretically inhibit the healing process.18 About 14 to 21 days after injury, glucocorticoids can control the inflammation and edema of the proliferative phase. The Achilles, patellar, and rotator cuff tendons should be avoided because direct injection into the tendon can place the patient at risk for rupture.18 The clinician must be careful to select a combination of medications within the recommended volumes to avoid further injury to the bursae. Table 11-1 may be used as a guideline for selecting the type and volume of corticosteroid and anesthetic to be administered.

Conclusion Bursal injections provide a useful diagnostic and therapeutic approach within a comprehensive rehabilitation program. The clinician should have a strong foundation in anatomy and must be

Table 11-1  Guidelines for Bursal Injections Needle Length (20-22 gauge, inches)c

Anesthetic Volumeb (mL)

Corticosteroid Volume (mL)

Subacromial

4.0-6.0

0.5-1.0

1.5

Trochanteric

4.5-9.0

1.5-1.0

1.5-3.5

Iliopectineal

4.0-4.5

0.5-1.0

3.5

Ischial

2.5-4.0

0.5-1.0

3.5

Anserine

2.5-4.5

0.25-0.5

1.5

0.5-1.0

1.5

Bursaea

Prepatellard aFluoroscopic

guidance may be necessary to increase accuracy of bursa injection. A bursogram may be a useful tool, increasing the diagnostic and therapeutic value of injections. bThe volume refers to the capacity of the bursa, and the clinician should select a corticosteroid concentration appropriate for the bursal volume. cThe clinician may prefer an 18-gauge needle initially for aspiration if gelatinous fluid is anticipated and then change to a finer gauge needle for instillation of pharmacologic agents. dThe prepatellar bursa is often multiloculated and its capacity may vary.

familiar with the pharmacologic agents. Diagnosing bursitis can be difficult with only a physical examination, and injection therapy is a useful diagnostic tool. Strong palpatory skills can aid in the injection process, verifying placement of medication into a superficial bursa such as the pes anserine. Fluoroscopic or ultrasound guidance can further ensure accurate delivery of medications to deep-lying bursae, avoiding unnecessary repeat injections due to an inaccurately placed needle. Injection therapy is neither a beginning nor an end point of a comprehensive rehabilitation program. Underlying biomechanical deficits of muscle weakness and tightness must be aggressively sought and corrected for an optimal result. REFERENCES    1. Smith DL, McAfee JH, Lucas LM, et al. Septic and non-septic ole­ cranon bursitis: Utility of the surface temperature probe in the early differentiation of septic and nonseptic cases. Arch Intern Med. 1989;149:1581-1585.   1a. Kelley WN, Harris ED, Ruddy S, Sledge CB. Textbook of Rheumatology. Philadelphia: WB Saunders; 1993: 545-560.    2. Kerr DR. Prepatellar and olecranon arthroscopic bursectomy. Clin Sports Med. 1993;12:137-142.    3. Waters P, Kasser J. Infection of the infrapatellar bursa. A report of two cases. J Bone Joint Surg Am. 1990;72A:1095-1096.    4. Magee DJ. Orthopedic Physical Assessment. Philadelphia: WB Saunders; 2008, p 706.    5. Vander Slam TJ. Atlas of Bedside Procedures. Boston: Little Brown; 1988: 455, 459, 461.   5a. Swezey RL. Pseudo-radiculopathy in subacute trochanteric bursitis of the subgluteus maximus bursa. Arch Phys Med Rehabil. 1976;57: 387-390.    6. Bach BR, Bush-Joseph C. Subacromial space injections: A tool for evaluating shoulder pain. Physician Sportsmed. 1992;2:93-98.    7. Nicholas JA, Hershman EB. The Upper Extremity in Sports Medicine. St. Louis: Mosby; 1995: 124-125.    8. Klippel JH, ed. Primer on the Rheumatic Diseases. Atlanta: Arthritis Foundation; 2008:143-146.    9. Ege Rasmussen KJ, Fanø N. Trochanteric bursitis: Treatment by corticosteroid injection. Scand J Rheumatol. 1985;14:417-420.   10. Collée G, Dijkmans BA, Vandenbroucke JP, Cats A. Greater trochanteric pain syndrome (trochanteric bursitis) in low back pain. Scand J Rheumatol. 1991;20:262-266.   11. Traycoff RB. “Pseudotrochanteric Bursitis”: The differential diagnosis of lateral hip pain. J Rheumatol. 1991;18:1810-1812.   12. Shbeeb MI, Matteson EL. Trochanteric bursitis (greater trochanter pain syndrome). Mayo Clin Proc. 1996;71:565-569.   13. Reid DC. Sports Injury Assessment and Rehabilitation. New York: Churchill Livingstone; 1992: 631, 1564, 1625–1626, 1636. 13a. Hemler DE, Ward WK, Karstetter KW, Bryant PM. Saphenous nerve entrapment caused by pes anserine bursitis mimicking stress fracture of the tibia. Arch Phys Med Rehabil. 1991;72:336-337.   14. Stuttle FL. The no-name, no-fame bursa. Clin Orthop. 1959;15:197-199. 14a. Lee JK, Yao L. Tibial collateral ligament bursa: MR imaging. Radiology. 1991;178:855-857.   15. Kerlan RK, Glousman RE. Tibial collateral ligament bursitis. Am J Sports Med. 1988;16:344-346.   16. Young JL, Press JM. Rehabilitation of running injuries. In: Buschbacher RH, Braddom RL, eds. Sports Medicine and Rehabilitation: A Sport-Specific Approach. Philadelphia: Hanley & Belfus; 1994:123-134.   17. Covino BG, Scott DB. Handbook of Epidural Anesthesia and Analgesia. Orlando: Grune & Stratton; 1985: 58-74.   18. Saal JA. General principles and guidelines for rehabilitation of the injured athlete. Phys Med Rehabil State Art Rev. 1987;1:523-536.

11

Tendon Sheath and Insertion Injections

12

Steve R. Geiringer, MD, and Ted A. Lennard, MD

Tendons are impressively strong structures that link muscles to bone. They function to transmit the force of muscular contraction to a bone, thereby moving a joint or helping to immobilize a body part. Their microscopic organization is thoroughly described elsewhere.1-3 The organizational unit in a tendon is the collagen fibril, which collectively forms fascicles, which as a group compose the tendon itself.4 Some tendons, especially long ones, are guided and lubricated along their paths by sheaths (Fig. 12-1) (e.g., biceps brachii, (Fig. 12-2) extensor pollicis brevis, and abductor pollicis longus). A prototypical muscle consists of the muscle belly centrally, two musculotendinous junctions, and tendinous insertions into bone at the points of anatomic origin and insertion.5 Some muscles, such as the extensor carpi radialis longus and brevis at the elbow, attach directly into bone (Figs. 12-3), an arrangement that may be more susceptible to injury.6 Much is known about a tendon’s response to laceration and operative repair,2 although this clinical situation is not frequently encountered. Less is understood about the more common and clinically relevant overuse tendinitis. A tendon and its sheath (if present) will undergo a typical inflammatory response to acute or chronic overuse injury, followed by a regenerative repair­ process.2,7,8 The distinction between an overload type of acute injury and a chronic overuse mechanism will aid in successful rehabilitation of tendinitis.9

Corticosteroid Injections Cortisone and its derivatives are known to reduce or prevent inflammation. Numerous corticosteroid preparations are available for local injection10 (see Chapter 2 on medications). The injectable corticosteroids are suspensions of insoluble particles, and therefore, the antiinflammatory effect is profound only where the material is deposited.11 The ability of corticosteroids to control inflammation makes them a valuable adjunct in treating tendon injuries because they do not alter the underlying process that leads to inflammation.10

Efficacy As with many other physical medicine treatment modalities, welldesigned scientific studies regarding the usefulness of corticosteroid injections are rare. These injections should be considered when, in

the practitioner’s judgment, the recognized antiinflammatory effect of local corticosteroid placement may be beneficial for the conditions of tendinitis, enthesitis, or tenosynovitis, and no harm will likely result. McWhorter and colleagues injected hydrocortisone acetate into rat Achilles peritenons that had been previously injured.3 There were no deleterious effects of one, three, or even five injections, measured biomechanically (tension to failure) or histologically (light microscopy), compared to controls. This finding should reassure physicians that they are not doing harm with properly placed steroid injections. A 30-year literature review identified eight prospective, placebo-controlled studies of steroid injection treatment for sports-related tendinitis.12 Three of the studies showed beneficial effects of injections at clinical follow-up. A metaanalysis of properly designed investigations of steroid injection for Achilles tendinitis found no beneficial effects,13 although very few studies qualified as rigorous. Adverse side effects occurred with a 1% incidence. No “proof ” of the usefulness or uselessness of this treatment modality exists.

Contraindications, Complications, and Side Effects The lack of a specific diagnosis is the single largest contraindication to a local corticosteroid injection. If the diagnosis is clear and the antiinflammatory effect of a corticosteroid may facilitate the rehabilitation process, injection can be considered.10 Repeated injections to the same area must be avoided, particularly into joints. Alterations in articular cartilage have been documented with repeated administration,14 possibly resulting in joint damage and weakened ligaments.15 A widely recognized complication of steroid injection is tendon rupture, a negative outcome that appears to be decreasing in frequency because it is now well understood. Achilles and other tendon ruptures have been reported,16-26 and deposition of injected material directly into any tendon substance is contraindicated. One report links the effect of repeated steroid injections to rupture of the ­plantar fascia.27 Some experimental findings have suggested that corticosteroid administration led to smaller, weaker tendons as a side effect.28 A more common side effect is subcutaneous atrophy, especially at the knee and lateral elbow and more frequently with the use of triamcinolone.10 Theoretically, atrophy of the specialized fat pads of the heel following steroid injection for plantar fasciitis may lead to a significant disability in an athlete, due to the loss of cushioning effect. 83

84  Soft Tissue and Joint Injections

B A

Figure 12-1  Drawing demonstrating a flexor tendon (A) within its sheath. The paratendinous septum is reflected (B).

R

A

L

A

R

B Figure 12-3  Common forearm extensor tendon at the lateral ­epicondyle— ultrasound evaluation. A, Longitudinal imaging of the common extensor tendon (arrows) and radial head (R). B, Longitudinal imaging of the common extensor tendon (arrowheads) demonstrating tendinosis (arrows) as hypoechoic swelling. L, Lateral epicondyle; R,radius. (From Jacobson J: Fundamentals of Musculoskeletal Ultrasound, Saunders, 2007, pp 110, 124.)

B Figure 12-2  Biceps brachii long head tendon ultrasound evaluation. A, Transverse imaging view over the biceps groove. Note transverse humeral ligament (arrowheads) and tendon. (arrows) B, Longitudinal imaging view of the biceps tendon in the anterior arm (arrows). (From Jacobson J: Fundamentals of Musculoskeletal Ultrasound, Saunders, 2007, p 42.)

Alternatives to Corticosteroids In recent years alternatives to corticosteroids have emerged for the treatment of chronic localized musculotendinous pain. These treatments include percutaneous tenotomies and platelet rich plasma (PRP) injections. Percutaneous tenotomies have been described for treatment of chronic lateral epicondylitis and plantar fasciitis.18,29 These injections are performed with large bore needles (18 or 20 gauge) under ultrasound guidance. The needle tip is used to repeatedly fenestrate the affected tissue under local anesthetic. The bony surface

(i.e.,  epicondyle) can be abraded and calcifications may be fragmented. This technique is thought to be a safe and effective alternative to corticosteroid injections.18,29 Platelet rich plasma injections use concentrated platelets from autologous blood to stimulate a healing response in damaged tissue. Blood is drawn from the patient and placed in a centrifuge. The concentrated platelets are removed and reinjected directly into the patient’s abnormal musculotendinous tissue or ligament usually under ultrasound guidance. These concentrated platelets produce growth factors that include platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and transforming growth factor-beta (TGF-β). These compounds are instrumental in attracting cells that promote healing by stimulating neovascularization and cellular reproduction.4,5,7,30 The efficacy of PRP injections and appropriate clinical indications (when and where it should be used) are currently being researched and yet to be definitively determined. Initial results of clinical studies appear promising.13,31,32

Methods of Injection Tendon and tendon sheath injections are office procedures, typically performed under clean or sterile conditions. The corticoster­ oid of choice is often combined with a local anesthetic, the latter

Tendon Sheath and Insertion Injections  85

12

helping to confirm the proper location of the deposited material. Diagnostic ultrasound has been advocated to guide injections near the heel when guidance by palpation alone fails.33 Immobilization of the treated structure usually is not needed following injection, although vigorous use of weight-bearing tendons (Achilles, patellar) should be avoided for 48 hours. Ice application may help when the local anesthesia fades, along with other physical medicine modalities as indicated by the particular condition present, usually starting after 48 hours. If an initial corticosteroid injection proves useful, one or two repeat injections separated by a few weeks or more may be considered. Numerous injections over time should not be considered the sole or primary treatment.

Indications Diagnosis Corticosteroid or local anesthetic injections should not be used routinely to arrive at diagnoses pertinent to the musculoskeletal system. The range of physical examination techniques used by the physician is described elsewhere34 and, in most cases, will suffice at pinpointing the specific cause of pain. The distinction between the conditions of subacromial bursitis and rotator cuff tendinitis can be clarified with injection,10 but even in this case the physical examination and subsequent rehabilitation program deservedly receive most of the attention.

Figure 12-4  Injection technique for first dorsal compartment stenosing tenosynovitis (de Quervain syndrome). The needle is parallel to the tendon.

Treatment In most instances, the literature supports an adjunctive, not primary, role for injections in the treatment of tendon and tendon sheath injuries.10,20 When the doctor and patient decide to proceed with injection, the control of inflammation that is obtained should be used to facilitate the prescribed rehabilitation program, rather than being the only treatment. The area of exception to this generalization is the wrist and hand (to be discussed in detail later). Upper Extremity Injections The literature supports the use of corticosteroid injections as a primary treatment for stenosing flexor tenosynovitis in the hand, known as trigger thumb or trigger digit.30,35-41 In this setting, injection has been shown to be as effective as operative release of the tendon sheath and to have fewer complications.42 Injection has been employed successfully into the hands of patients with diabetes mellitus and trigger digit, but the success rate may be reduced.43,44 Instillation of the material directly into the tendon sheath has no apparent benefit over subcutaneous placement.45 Multiple pulley rupture17 and flexor digitorum profundus and superficialis tendon rupture16 has been reported as a complication from this injection. As with other soft tissue injections, a physician treating trigger finger with instillation of corticosteroid needs to maintain expertise by performing this procedure at least several times yearly. Stenosing tenosynovitis of the first dorsal wrist compartment also is known as de Quervain syndrome. This compartment typically transmits the tendons of both the abductor pollicis longus (APL) and extensor pollicis brevis (EPB). However, anatomic studies have demonstrated that multiple APL slips are common, as are two subcompartments.39 Interestingly, although one or more injections are usually successful in treating de Quervain syndrome nonoperatively,22,46 patients requiring subsequent operative release

Figure 12-5  Injection technique for lateral epicondylitis. The needle tip is placed into the point of maximum tenderness at the edge of the bone.

have been found to have two subcompartments in greater than expected frequency.22,46 Trigger digit and de Quervain syndrome, therefore, are usually treated successfully nonoperatively, and corticosteroid injection is the primary component of the management (Fig. 12-4). The use of corticosteroid injection for lateral epicondylitis (tennis elbow) appears widespread (Fig. 12-5), although carefully controlled studies to confirm its efficacy are absent from the literature.47 One prospective investigation found that corticosteroid injection was more effective in controlling symptoms 8 weeks after injury than anesthetic alone, but the benefit disappeared by 24 weeks.29 This may be explained by the finding that the histology of tennis elbow is noninflammatory.48 A prospective chart review found that injection alone was effective in 91% of patients within 1 week, but was associated with a 51% recurrence after 3 months.

86  Soft Tissue and Joint Injections

Figure 12-6  Injection technique for long head of biceps brachii. The needle is directed parallel to the tendon.

Figure 12-7  Injection technique for plantar fasciitis. The needle tip is advanced to the insertion of the plantar fascia adjacent to the bone.

Initially, a standard physical therapy regimen led to improvement in only 74%, but the recurrence rate dropped to 5%.49 In the typical clinical setting, of course, injection(s) and physical therapy are often combined with careful consideration of the intrinsic and extrinsic biomechanical factors that may be contributors.9,50 No recent studies have examined the use of corticosteroid injections in the treatment of biceps brachii tendinitis. In this area, care should be taken to deposit the suspension to bathe the tendon sheath rather than into the body of the tendon itself (Fig. 12-6). Additionally, heavy lifting or vigorous exercise of the arm should be restricted for 48 to 72 hours following injection. Corticosteroid injection has been found to be effective for rotator cuff tendinitis—at least for the first several weeks. In one study, injection was superior to placebo and to oral antiinflammatory medication over the course of 4 weeks.51 No more than three injections are recommended.10 The technique itself is detailed elsewhere.11 After corticosteroid injection for treatment of rotator cuff tendinitis, heavy lifting and excessive overhead work are to be avoided for at least 2 days.

that includes flexibility training and correction of any contributing intrinsic or extrinsic biomechanical factors.10 If lipoatrophy occurs in the fat pad of the heel secondary to corticosteroid deposition, true disability in the active individual may result. Cosmesis is less of a problem because of the location. Most physicians are aware of possible tendon rupture if corticosteroid is injected directly into the Achilles tendon.34,52,53 On the other hand, the Achilles sheath can be injected,11 often with a good therapeutic result. One double-blind, randomized, controlled study found no advantage of Achilles tendon sheath injections when compared with standard physical therapy measures.54 Iliotibial band tendinitis, refractory to other measures, sometimes responds to corticosteroid injection. The material is placed around the insertion of the iliotibial band at the proximal, lateral tibia, or, depending on the site of symptoms, where it passes over the prominence of the lateral femoral condyle.10 Iliopsoas tendinitis has been similarly treated,55 with up to 2 years of symptomatic relief. The quadriceps (infrapatellar) tendon can be injected for cases of tendinitis,11 but because this is a weight-bearing structure, many practitioners avoid this procedure for fear of rupture.

Lower Extremity Injections The literature contains relatively few references to corticosteroid injections of the lower limb for tendon or tendon sheath injuries. In this arena, as in much of musculoskeletal medicine, the practitioner must rely on anecdotal evidence, clinical experience and judgment, and trial and error when choosing a course of treatment. Although it is not a true tendinitis, plantar fasciitis is commonly treated with steroid injection(s) (Fig. 12-7). If used, they must be considered complementary to a complete rehabilitation program

Conclusion In most cases of tendinitis or tenosynovitis of the upper or lower limb, corticosteroid injection for control of inflammation should be considered as a supplement to an individualized, well-designed, rehabilitation program. Notable exceptions are trigger digit or thumb, in which corticosteroid therapy is a successful primary intervention, and, to a lesser extent, de Quervain syndrome. The

Tendon Sheath and Insertion Injections  87

physician using corticosteroid injections must perform them often enough to maintain technical expertise. Three injections for any given injured area is considered a conservative maximum. Subcutaneous atrophy is a common side effect, and the known complication of tendon rupture strongly recommends against injections of corticosteroid directly into the substance of tendons. REFERENCES   1. Cooper RR, Misol S. Tendon and ligament insertion. J Bone Joint Surg Am. 1970;52:1-20.   2. Kennedy JC, Willis RB. The effects of local steroid injections on tendons: A biomechanical and microscopic correlative study. Am J Sports Med. 1976;4:11-21.   3. McWhorter JW, Francis RS, Heckmann RA. Influence of local steroid injections on traumatized tendon properties. A biomechanical and histological study. Am J Sports Med. 1991;19:435-439.   4. Menetrey J, Kasemkijwattana C, Day CS, et al. Growth factors improve muscle healing in vivo. J Bone Joint Surg Br. 2000;82:131-137.   5. Yasuda K, Tomita F, Yamazaki S, et al. The effect of growth factors on biomechancical properties of the bone-patellar tendon-bone graft after anterior cruciate ligament reconstruction: a canine model study. Am J Sports Med. 2004;32:870-880.   6. Brophy DP, Cunnane G, Fitzgerald O, Gibney RG. Technical report: Ultrasound guidance for injection of soft tissue lesions around the heel in chronic inflammatory arthritis. Clin Radiol. 1995;50:120-122.   7. Anitua E, Andia I, Sanchez M, et al. Autologous preparations rich in growth factors promote proliferation and induce VEGF and HGF production by human tendon cells in culture. J Orthop Res. 2005;23:281-286.   8. Badalamente MA, Sampson SP, Dowd A. The cellular pathobiology of cumulative trauma disorders/entrapment syndromes: Trigger finger, de Quervain’s disease and carpal tunnel syndrome. Trans Orthop Res Soc. 1992;17:677.   9. Fauno P, Anderson HJ, Simonsen O. A long-term follow-up of the effect of repeated corticosteroid injections for stenosing tenovaginitis. J Hand Surg Br. 1989;14:242-243. 10. Halpern AA, Horowitz BG, Nagel DA. Tendon ruptures associated with corticosteroid therapy. West J Med. 1977;127:378-382. 11. Curwin S, Stanish WD, Tendinitis. Its Etiology and Treatment. ­Lexington: Collamore Press; 1984. 12. Almekinders LC, Temple JD. Etiology, diagnosis, and treatment of tendonitis: An analysis of the literature. Med Sci Sports Exerc. 1998;30:1183-1190. 13. Mishra A, Pavelko T. Treatment of chronic elbow tendinosis with buffered platelet-rich plasma. Am J Sports Med. 2006;34(11):1774-1778. 14. Kerlan RK, Glousman RE. Injections and techniques in athletic medicine. Clin Sports Med. 1989;8:541-560. 15. Mankin HJ, Conger KA. The acute effects of intra-articular hydrocortisone on articular cartilage in rabbits. J Bone Joint Surg Am. 1966;48: 1383-1388. 16. Fitzgerald BT, Hofmeister EP, Fan RA, et al. Delayed flexor digitorum superficialis and profundus ruptures in a trigger finger after a steroid injection: A case report. J Hand Surg Am. 2005;30(3):479-482. 17. Gyuricza C, Umoh E, Wolfe SW. Multiple pulley rupture following corticosteroid injection for trigger digit: A case report. J Hand Surg Am. 2009;34(8):1444-1448. 18. Housner JA, Jacobson JA, Misko R. Sonographically guided pecutaneous needle tenotomy for the treatment of chronic tendinosis. J Ultrasound Med. 2009;28:1187-1192. 19. Leach R, Jones R, Silva T. Rupture of the plantar fascia in athletes. J Bone Joint Surg Am. 1978;60:537-539. 20. Minamikawa Y, Peimer CA, Cox WL, et al. De Quervain’s syndrome: Surgical and anatomical studies of the fibroosseous canal. Orthopedics. 1991;14:545-549. 21. Noyes F, Grood E, Nussbaum N. Effect of intra-articular corticosteroids on ligament properties: a biomechanical and histological study in rhesus knees. Clin Orthop Relat Res. 1977;123:197-209.

22. Peters-Veluthamaningal C, Winters JC, Groenier KH, et al. Randomised controlled trial of local corticosteroid injections for de Quervain’s tenosynovitis in general practice. BMC Musculoskelet Disord. 2009 Oct 27;10:131. 23. Reid DC. Connective tissue healing and classification of ligament and tendon pathology. In: Reid DC, ed. Sports Injury Assessment and Rehabilitation. New York: Churchill Livingstone; 1992:65-83. 24. Sweetnam R. Corticosteroid arthropathy and tendon rupture. J Bone Joint Surg Br. 1969;51:397-398. 25. Tonkin MA, Stern HS. Spontaneous rupture of the flexor carpi radialis tendon. J Hand Surg Br. 1991;16:72-74. 26. Velan GJ, Hendel D. Degenerative tear of the tibialis anterior tendon after corticosteroid injection-augmentation with the extensor hallucis longus tendon, case report. Acta Orthop Scand. 1997;68:308-309. 27. Kapetanos G. The effect of the local corticosteroids on the healing and biomechanical properties of the partially injured tendon. Clin Orthop Relat Res. 1982;163:170-179. 28. Geiringer SR, Bowyer BL, Press JM. Sports medicine. 1. The physiatric approach. Arch Phys Med Rehabil. 1993;74:S428-S432. 29. McShane JM, Nazarian LN, Harwood MI. Sonographically guided percutaneous needle tenotomy for treatment of common extensor tendinosis in the elbow. J Ultrasound Med. 2006;25:1281-1289. 30. de Mos M, van der Windt AE, Jahr H, et al. Can platelet-rich plasma enhance tendon repair? A cell culture study. Am J Sports Med. 2008;36(6): 1171-1178. 31. Sanchez M, Azofra J, Anitua E, et al. Plasma rich in growth factors to treat articular cartilage avulsion: A case report. Med Sci Sports Exerc. 2003;35:1648-1652. 32. Sanchez M, Anitua E, Azofra J, et al. Comparison of surgically repaired Achilles tendon tears using platelet-rich fibrin matrices. Am J Sports Med. 2007;35:245-251. 33. Becker C, Heidersdorf S, Drewlo S, et al. Efficacy of epidural perineural injections with autologous conditioned serum for lumbar radicular compression: an investigator-initiated, prospective, double-blind, ­reference-controlled study. Spine. 2007;32(17):1803-1808. 34. Dijs H, Mortier G, Driessens M, et al. A retrospective study of the conservative treatment of tennis elbow. Acta Belg Med Phys. 1990;13:73-77. 35. Anderson B, Kaye S. Treatment of flexor tenosynovitis of the hand (“trigger finger”) with corticosteroids: A prospective study of the response to local injection. Arch Intern Med. 1991;151:153-156. 36. Kalaci A, Cakici H, Hapa O, et al. Treatment of plantar fasciitis using four different local injection modalities: A randomized prospective clinical trial. J Am Podiatr Med Assoc. 2009;99(2):108-113. 37. Kerrigan CL, Stanwix MG. Using evidence to minimize the cost of trigger finger care. J Hand Surg Am. 2009;34(6):997-1005. 38. Kleinman M, Gross A. Achilles tendon rupture following steroid injection. Report of three cases. J Bone Joint Surg Am. 1983;65:1345-1347. 39. Lambert MA, Morton RJ, Sloan JP. Controlled study of the use of local steroid injection in the treatment of trigger finger and thumb. J Hand Surg Br. 1992;17:69-70. 40. Marks MR, Gunther SF. Efficacy of cortisone injection in treatment of trigger fingers and thumbs. J Hand Surg Am. 1989;14:722-727. 41. Taras JS, Raphael JS, Pan WT, et al. Corticosteroid injections for trigger digits: Is intrasheath injection necessary? J Hand Surg Am. 1998;23: 717-722. 42. Jeyapalan K, Choudhary S. Ultrasound-guided injection of triamcinolone and bupivacaine in the management of DeQuervain’s disease. ­Skeletal Radiol. 2009;38(11):1099-1103. 43. Nimigan AS, Ross DC, Gan BS. Steroid injections in the management of trigger fingers. Am J Phys Med Rehabil. 206;85(1):36-43. 44. Sibbitt WL, Eaton RP. Corticosteroid responsive tenosynovitis is a common pathway for limited joint mobility in the diabetic hand. J Rheumatol. 1997;24:931-936. 45. O’Brien M. Functional anatomy and physiology of tendons. Clin Sports Med. 1992;11:505-520. 46. Sawaizumi T, Nanno M, Ito H. DeQuervain’s disease: Efficacy of intrasheath triamcinolone injection. Int Orthop. 2007;31(2):265-268.

12

88  Soft Tissue and Joint Injections 47. Price R, Sinclair H, Heinrich I, et al. Local injection treatment of tennis elbow-hydrocortisone, triamcinolone and lignocaine compared. Br J Rheumatol. 1991;30:39-44. 48. Leadbetter WB. Cell-matrix response in tendon injury. Clin Sports Med. 1992;11:533-578. 49. DaCruz DJ, Geeson M, Allen MJ, Phair I. Achilles paratendonitis: An evaluation of steroid injection. Br J Sports Med. 1988;22:64-65. 50. Rineer CA, Ruch DS. Elbow tendinopathy and tendon ruptures: epicondylitis, biceps and triceps ruptures. J Hand Surg Am. 2009;34(3):566-576. 51. Adebajo AO, Nash P, Hazleman BL. A prospective double blind dummy placebo controlled study comparing triamcinolone hexacetonide injection with oral diclofenac 50 mg TDS in patients with rotator cuff tendinitis. J Rheumatol. 1990;17:1207-1210.

52. Galloway MT, Jokl P, Dayton OW. Achilles tendon overuse injuries. Clin Sports Med. 1992;11:771-782. 53. Shrier I, Matheson GO, Kohl HW 3rd. Achilles tendonitis: Are corticosteroid injections useful or harmful? Clin J Sports Med. 1996;6: 245-250. 54. Cyriax J. Textbook of Orthopaedic Medicine: Vol. 2. Treatment by Manipulation Massage and Injection. London: Baillière Tindall; 1980. 55. Vaccaro JP, Sauser DD, Beals RK. Iliopsoas bursa imaging: Efficacy in depicting abnormal iliopsoas tendon motion in patients with internal snapping hip syndrome. Radiology. 1995;197:853-856. 56. Warwick R, Williams PL. Gray’s Anatomy. 36th ed. Edinburgh: Churchill Livingstone; 1980.

13

Trigger Point Injections Ted A. Lennard, MD Trigger point injections (TIs) are helpful treatment options in patients with acute and chronic muscle pain often associated with underlying bone or nerve pathology. This chapter will discuss the differences in trigger points (TrPs) and tender spots (TSs), describe the three common types of trigger point injections, and discuss the specific techniques of these types of injections.

Trigger Points versus Tender Spots Trigger points (TrPs) are small, exquisitely tender areas in various soft tissues, including muscles, ligaments, periosteum, tendons, and pericapsular areas.1-1d These points may radiate pain into a specific distant area called a “reference pain zone.”1d-9 The referred pain may be present at rest. The pain may occur only on activation of the trigger point by local pressure, piercing by an injection needle, or activity of the involved muscle (particularly its overuse). TrPs located in muscles are called myofascial because they also may involve the fascia. In addition to the focal tenderness, they are characterized by the presence of a taut band6,8,9 that is sensitive to pressure, which indicates sensitization of the nerve endings within. The hard resistance to palpation and needle penetration is interpreted as evidence that a group of the affected muscle fibers is constantly contracted. Later, approximately 6 to 8 weeks after an injury, the resistance to the needle usually becomes very hard. This is characteristic of fibrotic (scar) tissues that fail to respond to conservative therapy. Because there are no definitive histologic studies of TrPs at different stages, it may be assumed that the damaged tissue has healed by a scar. Trigger point injections represent specific techniques used for alleviation of pain caused by the trigger area. Optimally, TIs are aimed at mechanically breaking up the entire abnormal tissue that causes pain. The most frequent findings related to pain are tender spots, a term reserved for point tenderness without radiating pain. TSs are frequently located within taut bands that have identical characteristics as TrPs. TIs have the same effect, indications, and limitations in both TSs and TrPs. Therefore, the rest of this chapter uses the expression “TrPs” for both tender spots and TrPs, because the technique of injection in both cases is identical: directed at the point of maximum tenderness and taut bands. Commonly, tender spots and some TrPs represent local tissue damage that causes inflammation and irritation that can be diagnosed by increased sensitivity to pressure. Figures 13-1 and 13-2 illustrate a possible concept of pathologic changes following local tissue damage. This hypothesis may explain clinical findings in acute and chronic injury and the effect of needling. Conceptually, the TSs

or TrP at the chronic stage can be thought of as a pocket of fibrotic tissue that contains sensitizing agents that are the products of tissue damage. These substances cause sensitization of the entrapped nerve fibers. This sensitization increases the nerve’s reactivity so that a lower pressure produces pain. Even without infiltration by anesthetic, the needling instantaneously abolishes the pain, tenderness, and fibrotic type of resistance. Such effect of dry needling can be best explained by breaking up a fibrotic pocket that has entrapped the nerve endings along with sensitizing substances. This allows the entering blood flow to wash away the sensitizing substances. This concept may explain the effect of TIs but has not been substantiated by histologic studies. Needling also may interrupt neuromuscular mechanisms involved in TrP activity. Figure 13-2 and Table 13-1 illustrate physical findings over TrPs and taut bands before, during, and after injection combined with needling. TrPs and TSs are the immediate cause of pain in a variety of conditions. These include sports or work-related injuries, sprains, strains, or muscle tension related to nonphysiologic posture or stress. Headaches also are frequently caused by TrPs. Certain hormonal disorders such as thyroid or estrogen deficiencies are frequent causes and perpetuators of widespread TrPs.

Trigger Point Injections Needling represents the most effective treatment of trigger points and TSs.9a-9f Injecting a local anesthetic (usually lidocaine) is combined with a special needling technique to break up the abnormal tissue that causes the pain. The critical factor in TIs is not the injected substance but rather the mechanical disruption of the abnormal tissue and interruption of the TrP mechanism if one has developed.2,10,11 Intensive stimulation also may contribute to the prolonged relief of pain by TrP injections.12 The fact that the symptoms originated in the treated TrP is confirmed by observing whether the pain is reproduced by pressure on the trigger area and relieved after the TrP injection.13 The injections are followed by a specific program of stretching and exercises. After fibrotic tissue (scar) has formed in the damaged tissue, the most effective way to break it up is through needling: the repetitive insertion and withdrawal of the injection needle in the affected area. Local anesthetics, such as 1% lidocaine or 0.5% procaine, provide temporary relief, lasting about 45 minutes. Long-term relief from pain is achieved by the needling, which mechanically breaks up the abnormal tissue.13a The number of injections needed depends on the number of TrPs present. 89

90  Soft Tissue and Joint Injections

1. ACUTE STAGE

Sprain Debris – contains inflammatory cascade substances that sensitize nerve endings, causing pain and sensitivity to pressure

Edema around the injured tissue Nerve endings within the damaged tissue are sensitized

Normal tissue

A Figure 13-1  Conceptual illustration of pathologic changes in acute tissue injury (A) that causes focal tenderness with pain.

One or two areas are usually injected during each treatment visit. Injections may be given 2 or 3 times a week for acute pain; once per week or once every 2 weeks is usually adequate as pain relief is being achieved. Each trigger point requires at least one injection. However, in large TrPs, injection may be limited to one segment per visit, depending on the patient’s tolerance. Sufficient tissue must be left around the needled areas for proper healing. Without proper treatment, TrPs tend to spread to additional muscles, causing flare-up of pain. The injection technique used for TrPs (combination of needling with infiltration) is effective in alleviating pain and restoring function in focal tenderness. The procedure is effective regardless of the underlying pathology and whether or not the pain is referred or limited to the tender area. Sprains and strains of muscles, ligaments, soft tissue injuries, inflammation, injuries of pericapsular tissues, and bursitis are the most common conditions that improve dramatically after needling combined with injection of local anesthetic. TrPs caused by endocrine dysfunction (especially thyroid or estrogen deficiency), fibromyalgia, psychological tension, or ischemia caused by muscle spasm also may be treated effectively by TIs. Often psychological tension and muscle spasm may not be alleviated without eliminating TrPs, which prevent relaxation of the muscle. Inability to relax tight muscles produces more TrPs, and a vicious cycle ensues.

The main contraindications for TIs include bleeding disorders, local infection, anticoagulant therapy, certain psychiatric conditions (anxiety, paranoia, schizophrenia), and inability to rest the injured body part following the procedure. Unless the conditions that caused the TrPs and perpetuating factors are diagnosed and treated, the TrPs will recur.

Common Trigger Point Injection Techniques Three commonly employed trigger point techniques include needling combined with infiltration of the entire taut band, technique of Travell and Simons, and injection of corticosteroids. There are some clinicians who have proposed ultrasound guidance in the cervicothoracic regions to prevent complications.13 1. Needling combined with infiltration of the entire taut band appears to be the most effective technique of TIs. Infiltration with a local anesthetic such as 1% lidocaine or 0.5% procaine is combined with needling. After withdrawal of the needle to the subcutaneous level, repetitive insertion and redirection of the needle is required to cover the entire abnormal (painful) area with as few skin penetrations as possible. The needling and infiltration is extended over the entire taut band, which

Trigger Point Injections  91

13 2. CHRONIC STAGE

Nerve endings

Fibrotic (scar) tissue forms, often creating a pocket that entraps the nerve endings and inflammatory substances, sensitizing them and causing pain

B Figure 13-1, cont’d.  Conceptual illustration of pathologic changes in chronic tissue injury (B) that causes focal tenderness with pain.

harbors the TrP/TSs, including its attachment to the bones (enthesopathy). 2. Technique of J. Travell and D.G. Simons.14-17 A small amount of 0.5% procaine is injected into the TrP to desensitize the most tender spot. This approach limits the needling and injection of 0.5% procaine to the most tender focus. The goal is to inactivate the neuromuscular TrP mechanism. The needling progresses in millimeters rather than centimeters, as described later. 3. Steroid injection. A 1.5-inch needle, usually 25-gauge, is used. Corticosteroids are combined with a small amount (1 to 3 mL) of local anesthetic, usually lidocaine. Corticosteroids are not necessary for myofascial TrP treatment. Precise needling, which breaks up the abnormal tissue, is more effective. In fact, corticosteroids may induce local myopathy. However, corticosteroids may be useful in the treatment of conditions involving passive tissues such as bursitis, tendinitis, epicondylitis, or ligament sprain. The disadvantages of corticosteroid injections into ligaments and tendons include loosening and incomplete healing. This may make the injected structures

more susceptible to reinjury. Also, the number of corticosteroid injections is limited to 3 to 5, leaving numerous TrPs untreated.

Trigger Point Injection Techniques The purpose of the injection is to mechanically break up the abnormal and sensitized, tender tissue by needling. Injection of any fluid adds to the mechanical effect of the procedure. Usually 1% lidocaine is optimal. However, in case of allergy to the “-caine” group, saline is satisfactory. The anesthetic also blocks pain and the irritation resulting from tissue damaged by the needle. The needle should be sufficiently long to be able to reach deeper than the trigger point. The diameter of the needle should be large enough to facilitate mechanical disruption of the abnormal tissue areas.18 A 22- to 25-gauge needle is usually sufficient. The total amount of 1% lidocaine injected ranges from 1 to 12 mL. Commonly, an extensive area must be infiltrated that ranges from 3 to 25 cm in length and 2 to 10 cm in width. The size of the infiltration depends on the extent of the trigger

92  Soft Tissue and Joint Injections

3. EFFECT OF NEEDLING-INJECTION

Needle Injected fluid Repetitive insertion of injection needle with infiltration breaks up the pocket of abnormal (fibrotic) tissue. This allows the blood circulation to wash away the irritative sensitizing substances.

C Figure 13-1, cont’d  The effect of needling that breaks up the abnormal tissue is also shown (C).

point and on the length of the affected muscle fibers. At each stop of the needle’s penetration, no more than 0.1 or 0.2 mL should be injected. Larger volumes can damage the muscle, negating any benefit.

Injection Procedure 1. Ask the patient to point out with one finger the area of most intense pain. If this pain is diffuse and corresponds to a trigger point’s reference zone(s), locate the TrP causing the symptoms.2,6,8,9 Palpate the muscle or ligament2 that has a corresponding reference zone. Position the patient so that you have proper access to the painful area. 2. Palpate the point of maximum tenderness. Mark it by impression of a fingernail. Palpate around to find the entire taut and tender band, which may reach from the origin to the insertion of the muscle, and mark it by fingernail impressions.

3. Explain the procedure to the patient. 4. Clean the skin with povidone-iodine or alcohol. Use surgical gloves. 5. Spray with ethyl chloride to frost. If patient does not like the vapo-coolant, pinch the skin in the area of injection and immediately insert the needle. Because the pinching distracts and occupies the sensory pathways, the patient does not feel the needle. 6. Needle the entire area where an increased fibrotic type of resistance is present, including the entire taut band. Explore with the needle beyond the border of the trigger point and the taut band. Inject only a small amount (0.1 to 0.3 mL) each time you stop the needle penetration. It is of great importance to always aspirate at each needle stop before the injection, especially when the neck or upper body is treated. Terminate the injection if blood is aspirated. 7. Proceed with the needle insertions through the taut band. Stop in 1 to 2 cm increments and again deposit only a small amount

Trigger Point Injections  93

13 BEFORE INJECTION: Normal muscle tissue: Elastic, soft resistance, nontender

TRIGGER POINT: Maximum tender point within the taut band

Measure with algometer

TAUT BAND: Hard and tender. Measure by tissue compliance meter and algometer AFTER INJECTION: The band and trigger point become soft and nontender.

Figure 13-2  Physical findings over a trigger point and taut band before, during, and after trigger point injection with needling.

Table 13-1  Physical Findings Before, During, and After Trigger Point Injections Before Injection

During Injection

After Injection

Minimal resistance to needle progression; no pain

Normal tissue findings

Penetration of the needle causes pain and encounters hard resistance as in fibrotic tissue (particularly in chronic TrP). Local twitch response occurs when the needle enters the hyperirritable fibers.

The hard and tender areas on palpation become nontender. Pressure pain sensitivity becomes normal immediately. Soreness from injection resolves in 3-5 days. Local twitch response can no longer be elicited. Hyperirritability resolves.

Maximum pain on needle penetration with hard resistance as in the taut band.

Trigger point sensitivity to pressure disappears. Hard consistency becomes normal, similar to improvement in taut bands.

Normal Muscle Tissue Elastic soft resistance; nontender Taut Band Hard and tender. Local twitch response can be elicited on snapping.

Trigger Point Maximum tender point within the taut band. TrP, Trigger point.

of anesthetic (0.1 to 0.2 mL) at each stop. When you reach the normal muscle below the taut band, the pain and hard resistance to the needle cease. Inject a smaller amount in the normal tissue and then withdraw the needle to the subcutaneous level. Make sure that the needle is out of the muscle when you

change the direction of the needle; otherwise, you will cut the tissue. Redirect the needle tip within the subcutaneous tissue along the plane of the taut band. Enter the band in distances 1 to 3 cm from the previous infiltration. The distance to the next insertion depends on the size of the muscle and the taut band.

94  Soft Tissue and Joint Injections

Proceed similarly until you needle and infiltrate the entire taut band. Depending on the patient’s tolerance, about 10 local infiltrations can be performed in one session, covering one large TrP and its taut band. If the patient becomes annoyed or the planned amount of anesthetic has been reached, the injection is terminated. If necessary, the remaining parts of the taut band can be injected in the following session, usually 1 week later. Immediately following an effective injection, the tenderness of the TrP and taut band, as well as the associated harder consistency of the surrounding tissue, disappears or diminishes substantially. Special attention should be directed to injecting the myotendon junction as well as the origin and the insertion of the involved muscle(s). Injection is usually particularly painful at these sites. Technique of injection to specific muscles has been described,4,8,9 and it is highly recommended that these textbooks are consulted before a novice starts TIs. 8. Compress the injected site for about 2 minutes to prevent bleeding. Cover area with an adhesive bandage.

Postinjection Care Postinjection care includes the following steps: 1. Promote hemostasis by pressure. 2. Encourage active slow movement of the injected muscle to its full range; repeat three times. 3. Apply heat locally. 4. Use physiotherapy consisting of hot packs and electric stimulation using sinusoid surging current (adjust volume to induce strong contractions that are not too painful). Use vapo-coolant spray to inactivate remaining painful areas. This is followed by limbering and stretching exercises. 5. If soreness is excessive, give acetaminophen or an NSAID. 6. Limbering exercises and/or passive stretching should be performed by the patient every 2 hours. Limbering exercises have been proven effective in preventing the recurrence of low back pain.19 Experience shows that this applies to all types of muscle pain. 7. Advise the patient to avoid heavy use of the injected muscle such as walking or driving long distances after lower body injections and to avoid sports after upper body injections.

Other Injections Currently, trigger point injections may be combined with other injection techniques such as preinjection blocks and paraspinous blocks. 1. Paraspinous block, which desensitizes the irritated spinal segment, is the first in sequence if spinal segmental sensitization is present. This is usually part of a cycle consisting of discopathy, radiculopathy, and paraspinal muscle spasm.10 The paraspinous block consists of two steps: (1) the spreading of the anesthetic (1% lidocaine) along the sprained (tender) supra/interspinous ligaments to achieve long-term healing and relief of spinal segmental sensitization; and (2) needling and infiltration of the sprained supra/interspinous ligaments.13

2. Preinjection block spreads anesthetic to prevent nociceptive impulses from the tender area to be injected.3,5,7 Preinjection block is administered before the injection of the tender area. The purpose is to block the pain sensation from the sensitive structure about to be injected. Preinjection block prevents central sensitization caused by injecting the irritative focus (a tender area) and also relaxes the neurogenic component of the taut band associated with the trigger point or tender spot.5 This makes the trigger point injection easier to perform and renders needling and infiltration more effective.5,7 REFERENCES   1. Fischer AA. Pressure threshold measurement for diagnosis of myofascial pain and evaluation of treatment results. Clin J Pain. 1987;2:207-214. 1a. Fischer AA. Documentation of myofascial trigger points. Arch Phys Med Rehabil. 1988;69:286-291. 1b. Kraus H. Diagnosis and Treatment of Muscle Pain. Chicago: Quintessence; 1988. 1c. Kraus H, Fischer AA. Diagnosis and treatment of myofascial pain. Mt Sinai J Med. 1991;58:235-239. 1d. Affaitati G, Fabrizio A, Savini A, et al. A randomized, controlled study comparing a lidocaine patch, a placebo patch, and anesthetic injection for treatment of trigger points in patients with myofascial pain syndrome: Evaluation of pain and somatic pain thresholds. Clin Ther. 2009;31(4):705-720.   2. Fischer AA. Quantitative and objective compliance recording. In: Nordhoff LS, ed. Motor Vehicle Collision Injuries. Gaithersburg, Md: Aspen; 1996:142-148.   3. Fischer AA. New approaches in treatment of myofascial pain. Phys Med Rehabil Clin North Am. 1997;8:153-169.   4. Fischer AA. New developments in diagnosis of myofascial pain and fibromyalgia. Phys Med Rehabil Clin North Am. 1997;8:1-21.   5. Fischer AA. Algometry in diagnosis of musculoskeletal pain and evaluation of treatment outcome: An update. In: Fischer AA, ed. Muscle Pain Syndromes and Fibromyalgia. New York: Haworth Medical Press; 1998:5-32.   6. Fischer AA. Treatment of myofascial pain. J Musculoskeletal Pain. 1999;7:131-142.   7. Fischer AA, Imamura ST, Imamura M. Myofascial trigger points are most frequently a manifestation of segmental spinal sensitization. J  Musculoskeletal Pain. 1998;6(Suppl 2):20.   8. Fischer AA, Imamura ST, Kaziyama HS, Imamura M. Trigger point injections and “paraspinous blocks” which relieve segmental spinal sensitization are effective treatment for chronic pain. J Musculoskeletal Pain. 1998;6(Suppl 2):52.   9. Frost FA, Jessen B, Siggaard-Andersen J. A control, double-blind comparison of mepivacaine injection versus saline injection for myofascial pain. Lancet. 1980;1:499-500. 9a. Deyo RA. Conservative therapy for low back pain. Distinguishing useful from useless therapy. JAMA. 1983;250:1057-1062. 9b. Fischer AA. Diagnosis and management of chronic pain in physical medicine and rehabilitation. In: Ruskin AP, ed. Current Therapy in Physiatry. Philadelphia: WB Saunders; 1984. 9c. Garvey TA, Marks MR, Wiesel SW. A prospective, randomized, ­double-blind evaluation of trigger-point injection therapy for lowback pain. Spine. 1989;14:962-964. 9d. Melzack R. Prolonged relief of pain by brief, intense transcutaneous somatic stimulation. Pain. 1975;1:357-373. 9e. Hackett GS. Ligament and Tendon Relaxation Treated by Prolotherapy. 3rd ed. Springfield, Ill: Charles C Thomas; 1958. 9f. Scott NA, Guo B, Barton PM, Gerwin RD. Trigger point injections for chronic non-malignant musculoskeletal pain: A systematic review. Pain Med. 2009;10(1):54-69.

Trigger Point Injections  95 10. Fischer AA. Local injections in pain management. Trigger point needling with infiltration and somatic blocks. Phys Med Rehabil Clin North Am. 1995;6:851-870. 11. Fischer AA. Injection techniques in the management of local pain. J Back Musculoskeletal Rehabil. 1996;7:107-117. 12. Fischer AA. Myofascial pain. In: Windsor RE, Lox DM, eds. Soft Tissue Injuries: Diagnosis and Treatment. Philadelphia: Hanley & Belfus; 1998:85-100. 13. Bonica JJ. Management of myofascial pain syndromes in general practice. J Am Med Assoc. 1957;164:732-738. 13a. Venancio Rde A, Alencar Jr FG, Zamperini C. Botulinum toxin, lidocaine, and dry-needling injections in patients with myofascial pain and headaches. Cranio. 2009;27(1):46-53. 14. Simons DG. Myofascial pain syndromes due to trigger points. In: Goodgold J, ed. Rehabilitation Medicine. St. Louis: Mosby; 1988.

15. Simons DG. Muscular pain syndromes. In: Fricton JR, Awad EA, eds. Advances in Pain Research and Therapy. New York: Raven Press; 1990. 16. Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual;Vol. I. Baltimore: Williams & Wilkins; 1983. 17. Tavell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. The Lower Extremities. Vol. II. Baltimore: Williams & Wilkins; 1992. 18. Yoon SH, Rah UW, Sheen SS, Cho KH. Comparison of 3 needle sizes for trigger point injection in myofascial pain syndrome of upper and middle trapezius muscle: A randomized controlled trial. Arch Phys Med Rehabil. 2009; 90(8):1332-1339. 19. Botwin KP, Sharma K, Saliba R, Patel BC. Ultrasound-guided trigger point injections in the cervicothoracic musculature: A new and unreported technique. Pain Physician. 2008;11(6):885-889.

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Botulinum Toxin Injections in Myofascial Pain Disorders

14

Hongtao Michael Guo, MD, PhD, Jodi J. Hawes, MD, PT, and Martin K. Childers, DO, PhD This chapter will discuss the uses of botulinum toxin for pain management in three of the myofascial pain disorders: cervical dystonia, myofascial pain syndrome and the piriformis syndrome. Although the uses for botulinum toxin that are licensed by the Food and Drug Administration (FDA) do not include pain management, it has been used by a range of medical specialists to address pain control of various etiologies. The purpose of this chapter is to provide clinical insights for clinicians regarding the use of botulinum toxin in three disorders that involve myofascial pain, based on the authors’ experience and literature review. As with all medications and procedures, clinicians must obtain the necessary training and knowledge to achieve the most effective and safe outcome. Accordingly, one should know essential features about this toxin before treating patients for pain. These vital elements include: mechanism of action1,2; concept of median lethal dose (LD50); dosing and administration3; basic neuromuscular anatomy and physiology; conjunctive therapy with botulinum toxin for optimal treatments;4,5 and contraindications, of using this toxin. Because it is beyond the scope of this chapter to address all of the topics just listed, the authors urge the reader to visit other informational sources listed at the end of this chapter.

Botulinum Toxin and Its Clinical Use Justinus Kerner, a German physician and poet, provided the first accurate and complete description of the clinical symptoms of food-borne botulism. He described 230 patients in the 1820s who suffered all the muscular and autonomic symptoms including gastrointestinal disturbances, dry eyes, dry skin, and weakness associated with the ingestion of contaminated meats.6 Kerner termed this condition “sausage poison” and “fatty poison”. He went on to perform animal experiments and experiments on himself. He administered botulinum toxin extracted from contaminated sausages to birds, cats, rabbits, frogs, flies, locusts, and snails.7 Kerner developed hypotheses from his experiments on the pathophysiology of the toxin. In his monograph he stated: “The nerve conduction is brought by the toxin into a condition in which its influence on the chemical process of life is interrupted. The capacity of nerve conduction is interrupted by the toxin in the same way as in an electrical conductor by rust.” Later in the monograph, he conceives of the idea of using the toxin for therapeutic uses.7 The term botulism was derived from the Latin term, “botulus”, which means sausage. Edward Schantz first isolated the toxin and he and Alan Scott began work on a standardized botulinum toxin

preparation in the late 1960s.6 Scott first used botulinum toxin type A in monkey experiments in 1973 and he first used botulinum toxin type A in humans to treat strabismus in 1980.6 Botulinum toxin type A was approved by the Food and Drug Administration (FDA) in 1989 for the treatment of strabismus, blepharospasm, and hemifacial spasm in patients more than 12 years of age. Botulinum toxin type B received FDA approval for treatment of cervical dystonia in 2000, and botulinum toxin type A was approved by the FDA to treat severe primary axillary hyperhydrosis and moderate-to-severe glabellar frown lines in 2002. In addition to the approved uses in the United States, there are other published uses of botulinum toxin,8 which include painful or potentially painful conditions such as: achalasia; anismus (painful); bladder detrusor hyperactivity; essential tremor; myofascial pain syndrome (painful); focal dystonias (sometimes painful); muscle spasm (often painful); piriformis syndrome (painful); spasmodic dysphonia; spasticity (sometimes painful); whiplash (painful); chronic focal painful neuropathies; migraines and other headache disorders; temporomandibular joint pain disorders; gastrointestinal dysmotility disorders; chronic low back pain. Aside from publications, noteworthy medical organizations have commented on the effectiveness and safety of botulinum toxin. The National Institutes of Health (NIH) Consensus Development Conference published a statement in 1990 that summarized the indications and contraindications of botulinum toxin usage for the treatment of a variety of conditions.9 The NIH conference endorsed the use of the neurotoxin as safe and effective for the symptomatic treatment of adductor spasmodic dysphonia, blepharospasm, cervical dystonia, hemifacial spasm, jaw-closing oromandibular dystonia, and strabismus. The same year, the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology further endorsed the use of botulinum toxin for the symptomatic treatment of these conditions.10 Botulinum toxin is held to be one of the deadliest poisons known to mankind, yet by harnessing this activity, it has resulted in great advances in the treatment of numerous conditions.2 The understanding of the mechanism of action of botulinum toxin had its beginnings in 1949 when Burgen’s group discovered that botulinum toxin blocks neuromuscular transmission.11 In the 1950s, researchers discovered that injecting overactive muscles with small quantities of botulinum toxin type A resulted in decreased muscle activity by blocking the release of acetylcholine (Ach) at the neuromuscular junction.11 The understanding of this mechanism of action led to the application of botulinum toxin in most clinical settings. Since 97

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then, significant advances have occurred in the understanding of the mechanisms of action of botulinum toxin other than muscle paralysis—and this is leading to additional applications. There are seven serotypes (A, B, C1, D, E, F and G) of botulinum toxin that act by inhibiting the exocytosis of Ach from presynaptic boutons of cholinergic neurons. Botulinum toxin is synthesized as a single-chain polypeptide (~150 kDa) that is activated by proteolytic cleavage into a 100-kDa heavy chain and 50-kDa light chain linked by a disulfide bond. The heavy chain domain is involved in cellular uptake into the presynaptic terminal by binding to extracellular receptors and in the transport of the neurotoxin through the lipid bilayer. The toxin is now intracellular but is sequestered in a membranous organelle without access to its targets, which reside in the cytoplasm. It is one of the functional domains (amino) of the heavy chain of the toxin that undergoes a conformational change facilitating translocation of the light chain through the lipid bilayer into the cytoplasm. Finally, the disulfide bond between the heavy and light chain is cleaved, allowing the light chain access to the cytoplasm. The light chain is a zinc-dependent endoprotease and the targets of the protease are presynaptic proteins required for intracellular trafficking of acetylcholine vesicles into the synaptic cleft. The presynaptic proteins targeted by the protease are called SNARE proteins (soluble N-ethylmaleimide-sensitive fusion protein attachment receptor) and are critical for the exocytosis of synaptic vesicles. It is this step, the proteolytic cleavage of the SNARE proteins, that is best understood in the intoxication by botulinum neurotoxin.12 The release of Ach into the synaptic cleft requires docking of the Ach-containing vesicle to the presynaptic membrane.12 The docking of the vesicle requires various proteins that are located in the wall of the vesicle, in the presynaptic membrane or in the cytoplasm. This family of proteins (SNAREs) includes vesicle-associated membrane protein (VAMP)/synaptobrevin, syntaxin, and SNAP25. These proteins form a complex that allows the vesicle to fuse with the motor nerve terminus membrane and release the acetylcholine into the synaptic cleft. The site of action of botulinum toxin type A is SNAP-25 (synaptosome-associated protein with a molecular weight of 25 kDa), which is a presynaptic membrane protein. Botulinum toxin type B targets VAMP (vesicle-associated membrane protein), which is located in the wall of the vesicle. Cleavage of the proteins prevents the assembly of the fusion complex and thereby blocks the docking of the vesicle and the release of the Ach leading to relaxation of the muscle cell and a state of chemical denervation.12 Of significant clinical importance is the duration of action of the toxin effect. In general terms, the clinical effects of botulinum toxin injections are delayed a day or two with the maximal effects of functional muscular weakness peaking at about 2 weeks.1,5 The therapeutic effect of botulinum toxin-induced neuromuscular blockade usually lasts 3 to 4 months and ranges 2 to 6 months following an injection.13 Several factors likely contribute to the duration of action of the toxin. The best understood factor and most often quoted is the synaptic remodeling; however, other factors such as the duration of protease activity in the nerve terminal, the rate of replacement of the cleaved SNARE proteins, and the activity of the cleavage products may also influence the rate of function recovery.6 The development of neutralizing antibodies to botulinum toxin can be a therapeutic problem for patients and physicians.14 Patients who initially respond well to treatment with botulinum toxin can become nonresponders.15 The incidence rates of neutralizing antibody development and the exact cause in individual

patients remains unknown.14 More frequent injections, more “booster injections,” and higher doses are possible risk factors, thus extending the time between injections, minimizing the dose, and avoiding booster injections may decrease the development of neutralizing antibodies.15 Some authors have noted that the pain relief preceded muscle decontraction and exceeded the degree and duration expected as a consequence of its neuromuscular actions.13 These observations suggest that botulinum toxin may have antinociceptive properties independent of the muscle relaxation. These observations and the expanding body of literature examining botulinum toxin for primary headache disorders and muscle conditions including a pain component led to further investigation into botulinum toxin in pain.16 A number of in vitro experiments have provided evidence that botulinum toxin inhibits neurogenic inflammation by attenuation of the release of neurotransmitters.17 Botulinum toxin was found to inhibit substance P release from cultured embryonic dorsal root ganglion neurons and to reduce stimulated release of calcitonin gene-related peptide from cultured trigeminal ganglia neurons.18 Additional support has come from animal experiments demonstrating reduction in nociceptive behaviors in animal models of inflammatory and traumatic neuropathic pain following peripheral injections of botulinum toxin.17 In rats with induced trigeminal neuropathy, intradermal injection of botulinum toxin in the area of the infraorbital branch of the trigeminal nerve alleviated the mechanical allodynia and reduced the exaggerated neurotransmitter release.19 In another experiment by Cui and colleagues, a rat formalin model of inflammatory pain was inhibited by subcutaneous administration of botulinum toxin injection and this inhibition was associated with a reduction in neurotransmitter release from the peripheral terminals of nociceptive sensory neurons. 20 It was Cui’s study in 2002 that provided the first evidence that botulinum toxin had an effect on nociceptive sensory nerves in vivo.20 In studies by Aoki, botulinum toxin inhibited several of the neurophysiologic and neurochemical effects of formalin in the rat formalin-pain model including glutamate release, Fos-LI in the dorsal horn, and evoked-activity of WDR neurons in the spinal cord.16 The efficacy of botulinum toxin in neuropathic pain initially was suggested in small anecdotal case studies and small open-label trials.21 An open study of botulinum toxin in 13 volunteers with trigeminal neuralgia found a reduction in visual analog scale scores and surface area of pain.22 Tsai and coworkers conducted an open label, prospective pilot study using botulinum toxin injected intracarpally in five patients with primary carpal tunnel syndrome.23 Their data suggested a long-acting antinociceptive effect of botulinum toxin. More recently, two well designed clinical trials evaluated the efficacy of botulinum toxin for chronic neuropathic pain and diabetic neuropathic pain.17,24 Ranoux and colleagues published a randomized, double-blind, placebo-controlled, parallel group study providing evidence in support of the efficacy of botulinum toxin for the pain associated with focal neuropathies such as postherpetic neuralgia and posttraumatic or postoperative neuropathy.17 The study included 29 patients with focal painful neuropathies and mechanical allodynia, and treatment consisted of a one-time intradermal administration of botulinum toxin into the painful area. Outcome measures included average spontaneous pain intensity, quantified testing of thermal and mechanical perception of pain, allodynia to brush and decreased pain threshold to cold; the measures were evaluated at baseline, 4, 12, and 24 weeks. The results

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indicated that botulinum toxin treatment, relative to placebo, was associated with persistent effects on spontaneous pain intensity from 2 weeks after the injection to 14 weeks.12 A recent study by Yuan and associates report the results of a double-blind, placebo-­ controlled, crossover trial of intradermal botulinum toxin for diabetic neuropathic pain in 18 patients.24 The authors found a signi­ ficant reduction in visual analog scale of pain at 1, 4, 8, and 12 weeks after botulinum toxin injection when compared to the placebo group. Specifically, within the botulinum toxin group, 44.4% of the participants experienced a reduction of the visual analog scale greater than or equal to 3 within 3 months after the injection, in contrast to the placebo group that reported no similar response. In addition, the authors evaluated sleep quality using the Chinese version of the Pittsburgh Sleep Quality Index and found a difference in the improvement in sleep quality between the botulinum toxin treatment group and the placebo group. The difference between the groups reached significance (P < .05) only 4 weeks after the initial injection, but did not support sleep improvement with botulinum toxin at week 12, which was the endpoint of the study design.24 Both reports (Yuan and colleagues24 and Ranoux and associates17) are small studies but each support a trend of reduced pain perception beginning at 1 week postinjection and extending to 12 weeks in the Yuan and colleagues’ study and 14 weeks in the Ranoux and associates’ study.17,24 Both studies report essentially no adverse events and this is supported by the general botulinum toxin literature. Although this suggests a promising approach to the treatment of neuropathy, additional larger, well designed, multicenter clinical trials with longer periods of follow-up are necessary.

Cervical Dystonia Cervical dystonia (CD), also known as spasmodic torticollis and torsion dystonia, is a common form of focal dystonia manifesting as involuntary contraction and twisting of the neck muscles.25,26 These features lead to abnormal postures and movements of the head. The deviation of the head can be multidirectional and is described as torticollis (the most common form of CD with patient’s head turned to one side); laterocollis (lateral flexion of the neck), anterocollis (flexion of the neck) and retrocollis (extension of the neck). It is possible that one can have a combination of these forms. The prevalence of CD was reported to be 8.9/1,000,00027 and it is recently estimated by the Dystonia Medical Research Foundation that 250,000 people suffer from CD in the United States. It is believed that 66% to 75% of the patients with CD are disabled from the pain associated with CD.27-30 CD is mostly idiopathic and about 12% of those affected have a family history.31 Idiopathic CD is the most common form of adult-onset focal dystonia slowly developed over several years in patients 30 to 50 years old.32 Cervical dystonia can be caused by any injury or inflammation of the cervical muscles or cranial nerves from various disease processes, including head, neck, and shoulder trauma33 or from taking dopaminergic block agents.34 There is evidence indicating that CD arises from basal ganglia circuit abnormalities leading to dopaminergic dysfunction, which in turn causes disinhibited thalamocortical output and dystonic postures.31,35-37 Patients with CD can have a wide spectrum of symptoms involving the head, neck, upper extremity, and other body parts with sustained painful muscle contraction, pulling, and/or stiffness.28,31,37 The severity of the pain is usually relative to the intensity of the dystonia and muscle spasms.28 Jahanshahi and colleagues reported progression of dystonic symptoms to extranuchal, but still

cervical, innervated sites such as hand, arm, and oromandibular region in one third of the 72 patients with adult-onset cervical dystonia.38 Patients with CD may develop neck pain from the muscle contraction and muscle strain from correcting the abnormal posture. The chronic abnormal posture may also lead to degenerative changes in the cervical spine leading to facet pain, radiculopathy, or spinal stenosis. Headaches associated with CD are common.39 Acute posttraumatic CD is different and the symptoms include immediate local pain after trauma, followed by a significant limitation in cervical range of motion, and abnormal posture of the head and shoulder. Trapezius hypertrophy may occur as well. Those changes often result in abnormal muscle contraction and pain.28,31 The abnormal posture and pain in patients with CD are part of their functional limitation and interfere with the patients’ activities of daily living.31 Rondot and coworkers40 found that 99% of the 220 patients they studies had various functional difficulties. Dysphasia and subclinical swallowing motility disturbances were reported in those patients.41 Permanent disability from the decreased cervical range of motion, involuntary movements, and intractable pain may occur.42 The diagnosis of CD is clinical and inspection is usually enough. However, a though physical examination should be conducted to rule out “pseudodystonia” due to structural abnormalities43 and secondary dystonia.

Treatment of Cervical Dystonia with Botulinum Toxin There are various treatment options for CD including medications,32,44-47 surgery,48-56 rehabilitation,57 deep brain stimulation,58,59 and injections. The goal of the treatments is to reduce the discomfort and pain; improve function and quality of life; and prevent complications. Other than botulinum toxin (BTX) injection, the other treatment modalities are beyond the scope of this chapter. The care of CD patients was drastically improved since 1989 when botulinum toxin was introduced in the United States. The FDA approved the indication of botulinum toxin injection for CD treatment in 2000. It is generally considered that BTX injection is the treatment of choice for patients with CD.60-62 The effectiveness of local injections of botulinum toxin is supported by evidencebased reviews and meta-analysis.45,54,63,64 Jankovic and Schwartz65 followed 202 out of 232 patients who received botulinum toxin type A injection for medically intractable CD for at least 3 months and up to 4 years. Seventy one percent of those patients had improved symptoms and 76% had almost complete relief of pain. Hsiung and colleagues published that 63% of patients treated with botulinum toxin injection reported benefit at 5 years.66 In a 20-week multicenter double-blind, randomized, controlled study in the United States involving 80 patients, the botulinum toxin group demonstrated improvement in the total Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS) score than did the placebo group at weeks 4, 8, and 12 weeks.67 The side effects of the two groups were similar except for blurred vision and weakness in the botulinum group. The Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology concluded that botulinum toxin is safe and effective for the treatment of CD.68 There are numerous studies using botulinum toxin type B for CD treatments.69-71 Pappert and Germanson compared the CD treatment with botulinum toxin type A and botulinum toxin type B in a randomized, double-blind study, and found that both types of botulinum toxin are effective and safe for the treatment of CD in botulinum toxin-naïve patients.72 There is disagreement regarding

14

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the study conclusion.73,74 In a Cochrane Reviews, Costa and associates concluded that single injections of botulinum toxin type A and type B are effective and safe for treating CD, and long-term, uncontrolled studies suggested that further injection cycles continue to work for most patients.63,75 In another Cochrane Review, these authors concluded that it was not possible to make a definitive comparison between botulinum toxin type A and type B for CD treatment.76 Because of the complexity of the neck, it is critical for the clinician to be familiar with the anatomic landmarks, the vital structure, and the muscles for a successful treatment of CD with botulinum toxin injection. Attention should be paid to the following structures/ organs when injecting botulinum toxin: the brachial plexus, carotid sheath, pharynx, esophagus, and the apex of the lung. The muscles involved in various forms of CD are listed in Table 14-1. Although the use of electromyography (EMG) for botulinum toxin injection for CD management remains controversial,68 the authors recommend using EMG-guided injection whenever possible to ensure the effective targeting of the affected muscles77 and the motor end plates within those muscles78-80 to potentiate neurotoxin effects. It is essential to have the patients as relaxed as possible to eliminate the false motor action potentials on EMG. If palpation alone is used to identify affected muscles, injection into either the mid-belly or several sites of the muscle is generally recommended. Because of the variation of muscle involvement, there are no clear guidelines for the appropriate dose of botulinum toxin for the treatment of CD. A wide range of dosages was reported in CD treatments with botulinum toxin type A81-90 and type B.69-71 Dressler found that 20 units of botulinum toxin type A reduced the dystonic activity in the sternocleidomastoid muscle and larger doses offered minimal additional effect.91 Koller and colleagues92 noted that fixed-dose, fixed-muscle controlled studies of botulinum toxin for the clinical management of CD did not produce the same effects. Based on our experiences and the literature review, we think that, in general, patients should receive as few doses of botulinum toxin as possible as long as their symptoms are managed; the dose of botulinum toxin should be individualized; and the lowest effective

Table 14-1  Typical Muscles Involved in Various Types of CD CD Type

Muscles Involved

Torticollis

Ipsilateral splenius (Spl)/semispinalis capitis (SC) Contralateral sternocleidomastoid (SCM)

Laterocollis

Ipsilateral SCM Ipsilateral Spl/SC Ipsilateral scalene complex Ipsilateral levator scapulae (LS) Ipsilateral posterior paravertebrals

Retrocollis

Bilateral Spl/SC Bilateral upper trapezius (trap) Bilateral deeper paravertebrals

Anterocollis

Bilateral SCM Bilateral scalene complex Bilateral submental complex

Shoulder elevation

Ipsilateral LS Ipsilateral trap

CD, Cervical dystonia. Adapted from Brashear A: Botulinum toxin type A in the treatment of patients with cervical dystonia. Biologics 3:1-7, 2009.

dosage of botulinum toxin should be administered for treatment of CD to protect the patient from becoming immune to its therapeutic effect.93,94 The side effects associated with botulinum toxin injections for CD include dysphagia, neck muscle weakness, nausea, generalized malaise, and pain, which is the most frequent side effect due to the local injection. Severe pain may occur when botulinum toxin is injected directly into or around a peripheral nerve. Typically, these side effects are temporary and should resolve in few weeks. However, any complications should be addressed accordingly. For instance, patients with an underlying swallowing disorder should be approached with caution when botulinum toxin injection is considered. Swallowing studies are helpful in detecting patients at risk or evaluating patients who develop dysphagia after injections. Diet modification may be necessary to avoid aspiration. Patient may develop excessive weakness in the neck following injection. Thorough evaluations are warranted and supportive measures, such as a cervical collar, may be needed for the weakened muscle groups. Pain may be treated with over-the-counter analgesics and opioid medications are rarely needed.

Myofascial Pain Syndrome Myofascial pain syndrome (MPS) is a painful disorder that is characterized by the presence of the palpable taut band of muscle fibers and myofascial trigger points (MTrP).95 The International Association for the Study of Pain defines the trigger point as a discrete tender point palpable in the taut muscle band.96 A myofascial pain syndrome caused by MTrPs characteristically results from either an acute episode of muscle overload or a chronic and/or repetitive muscle overload.97 In addition, there are autonomic phenomena (piloerection, localized sweating, or even regional temperature changes in the skin because of altered blood flow), concomitant disorders, psychosocial factors, and psychiatric presentations including depression and anxiety.98,99 There are different opinions about what MPS represents. Some scholars think that it should cover all the regional pain caused by any soft tissue pathology. Thus, MPS may be considered as a primary local or original pain syndrome or a secondary syndrome caused by other disorders.100,101 Research studies indicate that the clinical characteristics of an MTrP can be explained by hypercontracted muscle fibers located at and produced by a region of muscle with multiple dysfunctional motor end plates (neuromuscular junctions). The dysfunction is a markedly excessive continuous release of the normal synaptic transmitter, Ach. The noise-like potentials and spikes that are strongly associated with MTrPs102-104 were first interpreted as coming from muscle spindles.103 However, electromyographic studies clearly identify these noise-like and spike potentials as motor endplate potentials of skeletal muscle fibers.105 Electromyographers generally recognize these end-plate potentials as normal.105-108 However, physiologists have distinguished these potentials from normal miniature end-plate potentials and have shown that they represent a pathologic increase in spontaneous release of Ach.109-112 The endplate noise component can result from mechanical strain of the neuromuscular junction caused by stresses applied to the nerve terminal112 or produced by muscle overload. The end-plate noise component of end-plate potentials appears to be present before the needle examination and is commonly caused by stressful activity of the muscle, especially in latent MTrPs that cause no clinical pain complaint. The end-plate spikes, however, are often induced by

Botulinum Toxin Injections in Myofascial Pain Disorders  101

the presence of the needle113 and are more likely to appear in more active MTrPs. Histologically, MTrPs show large, darkly stained, round myofibers in cross section in canine,114 equine115 and in human116,117 studies. Longitudinal sections of myofibers several hundred microns in length of canine muscle show hypercontracted fibers (also called “contraction knots”). The integrated hypothesis for the pathophysiology of MTrPs attributes these contraction knots to the observed depolarization of the post-junctional membrane that continuously releases calcium from the sarcoplasmic reticulum. This hypothesis identifies contraction knots as limiting circulation because the strong contraction of the sarcomeres is sustained within the hypercontracted fiber, whereas local energy consumption is increased. The resulting energy crisis should exhibit severe local hypoxia, demonstrated in the MTrPs.118 Increased tension of involved muscle fibers accounts for the palpable taut band consistently associated with an MTrP. The energy crisis and local hypoxia that was observed to extend for several millimeters could account for the release of substances that sensitize local nociceptors, causing the local and referred pain characteristic of MTrPs.97 An interesting study examined rabbit muscle after a marker (iron deposit) was placed at precisely the location where an active trigger point was identified by twitch response, taut band, and spontaneous electrical activity. Small C nerve fibers (most likely nerves that carry pain information) were found in the immediate vicinity.107 Taken together, these data support the idea that MTrPs are related to abnormal motor end-plate activity and subsequent hypercontraction of the associated myofibers.119 MTrPs are identified on physical examination by palpating a localized tender spot in a nodular portion of a taut band of muscle fibers. Pressure (usually with the examiner’s fingertip) over a trigger point elicits pain at that area and may also elicit pain at a distance from the point under the fingertip. This is known as referred pain. Another important feature of the trigger point is that the elicited pain mirrors the patient’s experience. Insertion of a needle, snapping palpation, or even a brisk tap with the fingertip directly over the MTrP may elicit a brief muscle contraction detectable by the examiner. This brisk contraction of muscle fibers of the taut band is termed a local twitch response.97 There is a burst of electrical activity within the muscle band that has the twitch response (end-plate noise), and such activity is not observed in the other muscle bands. This type of end-plate noise is found more prevalently in myofascial trigger points than in sites that are outside the MTrP but still within the end-plate zone.120 Animal studies102,121,122 and a human study123 have shown that this response is propagated as a spinal reflex. This response is a valuable indicator that the needle being injected into an MTrP has effectively reached at least one necessary target in the MTrP. Demonstration of a local twitch is additional confirmation of the diagnosis. In addition, passive stretch range of motion of the muscle is limited by pain, and both maximum contraction in the shortened position and maximum voluntary contraction are likely to be inhibited or to be associated with pain. If abnormal end-plate activity is responsible for MTrPs, then a powerful rationale exists for the use of neuromuscular blocking agents, such as botulinum toxin, in the treatment of myofascial pain syndrome.124 Injection of muscles with botulinum toxin can be appropriate therapy for myofascial pain caused by MTrP but is unlikely to be so for treatment of myofascial pain of unspecified origin, when that term is used in the general sense.125 Myofascial pain with muscle tenderness versus specific MTrPs responsible for the clinical pain is an ambiguous diagnosis. The tender spots may

be due to fibromyalgia, bursitis, or one of many other diagnoses that do not justify injection with this product. At present, no routine laboratory test or routine imaging test is available to confirm the presence of MTrPs. Usually two objective tests can be used to confirm the presence of MTrPs. One requires electrodiagnostic technique and the other uses ultrasound imaging. Both animal and human research studies have shown that MTrPs are characterized by electrically active loci that exhibit end-plate noise and often spikes.107

Treatment of Myofascial Pain Syndrome with Botulinum Toxin The previous chapter in the second edition included a Medline search conducted in 1997 for the headings “botulinum toxin,” “myofascial pain,” and “pain” for the period 1966 to September 1997 and resulted in 18 references.126 An updated Medline search for the period September 1997 to April 2009 was conducted using the headings “botulinum toxin” and “myofascial pain syndrome” and resulted in 45 references. Of these, 21 studies were in English and included “pain” or “myofascial pain” within the article title.127-147 A few words of caution before considering using botulinum toxin in the treatment of a patient with myofascial pain: Recall that the approved indications for the use of botulinum toxin in the United States are for six conditions: strabismus, blepharospasm, hemifacial spasm, cervical dystonia, primary axillary hyperhidrosis, and moderate-to-severe glabellar frown lines.6 Use of botulinum toxin for myofascial pain is off-label and should be considered only for patients with conditions that failed conservative treatment or for patients judged inappropriate for conservative treatment.145 Two studies were designed to compare trigger point injections in the management of patients with myofascial pain and headaches.127,135 The studies included a total of 74 patients that were randomly assigned to one of three groups: dry needling, lidocaine injection, or botulinum toxin injection. Venancio and colleagues assessed their subjects during a 12-week period based on levels of pain intensity, frequency and duration, local post-injection sensitivity, obtainment time and duration of relief, and the use of rescue medication.127 In contrast, Kamanli and coworkers’ assessment measures included cervical range of motion, trigger point pain pressure threshold, pain scores, visual analog scales for pain, fatigue, and work disability at entry and at 4 weeks.135 In addition, depression, anxiety, and quality of life were assessed. Venancio and coworkers found that, statistically, all the groups showed favorable results for the evaluated requisites, except for the use of rescue medication and local post-injection sensitivity (botulinum toxin group showed better results). Similarly in the study by Kamanli and coworkers, all three groups showed a significant improvement in pain pressure thresholds and pain scores; however, the lidocaine injection group’s pain pressure threshold values were significantly higher than the dry needling group and their pain scores were significantly lower than either the dry needling or botulinum toxin injection groups.135 Both studies concluded that lidocaine could be adopted as a substance of choice considering its reduced cost and botulinum toxin should be reserved for refractory cases. A study by Porta compared the effects of botulinum toxin type A with the steroid methylprednisolone in146 patients with chronic myofascial pain in the piriformis, iliopsoas, or scalenus anterior muscles.146 Both groups of patients had a significant pain reduction at 30 days post-injection but there was no significant difference

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between the groups. At 60 days following the injection the pain scores were statistically significantly lower in the botulinum toxin group when compared to the steroid group. In addition, the pain scores in the botulinum toxin group were lower at 60 days than at 30 days post injection.146 Six of the twenty-one studies had “myofascial pain syndrome” and “neck” or “back” pain in the title including a review by Porta and Maggioni.128,132,134,136,139,148 Gobel’s report was a randomized, double-blind, placebo-controlled, multicenter study including 145 patients with moderate-to-severe myofascial pain syndrome affecting cervical and/or shoulder muscles.132 The injections were made into the 10 most tender trigger points (40 units per site). Compared to placebo, botulinum toxin resulted in more patients with mild or no pain at week 5, a significantly greater change from baseline in pain intensity during weeks 5 through 8, and significantly fewer days per week without pain between weeks 5 and 12.132 Another randomized, double-blind, placebo-controlled study with 29 subjects with neck and upper back pain of myofascial origin compared botulinum toxin injections to placebo (saline injections).148 The botulinum toxin injection used 50 units and the outcome measures were the visual analog scale for pain, the neck disability index, and the medical outcome study 36-item short form health survey.148 Improvements were seen in the visual analog scale and the neck disability index but were not significant when compared to the controls. The outcomes as measured by the 36-item bodily pain short form and the 36-item mental health short form did reach statistical significance in the treatment group at 2 and 4 months and at 1 month, respectively.148 Braker and colleagues evaluated the effectiveness of botulinum toxin injections compared to placebo in 20 patients with cervical myofascial pain following a whiplash injury (2 to 48 weeks following injury).128 Subjects received 200 units of botulinum toxin or placebo at four tender points and were seen in follow-up at 3, 6, 9, 12, and 24 weeks.128 Outcome measures included pain intensity evaluated by the visual analog scale and verbal rating scale, quality of life measured by the SF-36 questionnaire, treatment efficacy as per the global assessment of the physician and patient, and intensity of pain response to mechanical pressure and cervical range of motion. Both groups had a time-dependent improvement in all parameters, which was consistently larger in the botulinum toxin group, although it did not reach significance.148 Wheeler and colleagues conducted a randomized, doubleblind study comparing the effects of botulinum toxin injections to normal saline in 33 subjects randomly assigned to either 50 or 100 units of botulinum toxin or normal saline.136 The subjects were evaluated over a 4-month period by assessment of pain and disability and pressure algometer readings. This study did not find any statistically significant benefit of botulinum toxin over placebo.136 The trial by Ojala and colleagues was designed to determine the effect of small doses of botulinum toxin (5 units per site).134 The authors found that no statistically significant changes in neck pain and pressure pain threshold values occurred between the low-dose botulinum toxin and saline groups. Ferrante and his colleagues149 conducted a randomized, double-blind, placebo-controlled study with 132 patients with cervicothoracic myofascial pain with trigger points. They concluded that the injection of botulinum toxin type A directly into the trigger points did not improve the cervicothoracic myofascial pain. In a comment on this study, Abram indicated that the negative results of the study by Ferrante and colleagues149 were unexpected because there is reason to predict reduction of pain given the pharmacologic effects attributed to botulinum toxin.150 He commented the notion from Ferrante and colleagues149 that the

site of trigger point injection may not be the optimal site for botulinum toxin injection of the muscle. Abram150 stated that although the motor end plate is the most effective location for injection and the site is not known for many of the muscles in myofascial pain, botulinum toxin should diffuse throughout the muscle and provide some effect at the higher dose of the study.150 He also expressed his concern about the accuracy of the diagnosis and the possible heterogeneity of the cohort selected in the Ferrante and colleagues’149 study. Abram150 stated that not all patients with muscle tenderness have myofascial pain syndrome; and some patients’ myofascial pain can be secondary to other painful disorders such as radiculopathy, facet arthropathy, or complex regional pain syndrome, which are much more resistant to treatment than primary myofascial pain syndrome. He suggested selecting patients who experience complete but temporary relief from local anesthetic trigger point injection for botulinum toxin injection or study.150 The authors think that Abram’s opinions are validated and they could be applied to other studies or treatments using botulinum toxin for patients with myofascial pain syndrome. A consensus statement on botulinum toxin in myofascial pain by Reilich and colleagues states that botulinum toxin should be considered if the patient has an assured chronic myofascial pain syndrome that has been resistant to less invasive measures.138 Their conclusions state that botulinum toxin injections should be performed in institutions with extensive experience in therapy of myofascial pain and treatment with botulinum toxin. Furthermore, the injections should be part of a multimodal therapeutic program including physical therapy and relaxation exercises. Thus, botulinum toxin injections seem to be an effective supplemental treatment, although the authors state further clinical evidence is needed from double-blind controlled trials.138 In MTrP injection, targeting is critical for attaining optimal and effective therapeutic goal. The trigger point injection (TPI) with botulinum toxin is similar to the TPI with other agents. Most practitioners use the direct injection technique. The skin overlying the MTrP is prepped and a needle is advanced to the point of maximum tenderness. Usually this will reproduce the patient’s myofascial pain or the referred pain. The botulinum toxin is injected after negative aspiration for blood. Usual side effects as with other forms of botulinum toxin injection and TPI may occur, although the risks are fewer. Lang reported a novel grid-pattern technique for injecting botulinum toxin in myofascial pain.151 He reported that 65% of the 72 patients had good-to-excellent pain relief, whereas 24% had fair, and 12% had poor pain relief. Of note, the median dose of botulinum toxin used in this study was 200 units. If the initial acute MTrP pain was not properly diagnosed or not treated effectively, it may lead to the chronic myofascial pain syndrome. The unresolved perpetuating mechanical or systemic factors may maintain the chronicity of the myofascial pain.97 Injecting these chronic MTrPs with botulinum toxin (or other agents) can be expected to provide relief only for a limited time if the perpetuating factors are not identified and resolved. It is important to remember that the commonly occurring, acute, single MTrP often reverts from active to latent MTrP without specific treatment if the individual simply avoids the muscle overload situation that activated the MTrP and proceeds with daily activities within limits that are not painful. This daily activity, which includes actively stretching the involved muscle gently but repeatedly, is an effective treatment. The recovery from acute MTrP syndromes is expedited and the likelihood of lasting relief is greatly improved if the patient learns to perform slow, gentle, active, full range-of-motion exercises

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specifically for the involved muscles at least once daily. Following injection of chronic MTrPs, the authors consider these exercises essential for optimum results.

Piriformis Syndrome Piriformis syndrome (PS) is a myofascial pain disorder that manifests with a spectrum of symptoms, including buttock pain, referred pain to the ipsilateral lower extremity, and/or low back pain, caused by piriformis muscle inflammation, spasms, contracture, anatomic anomalies, or irritation to the sciatic nerve.152-154 The piriformis is from the Latin words pirum (pear) and forma (shape). It is a flat muscle originating from the anterior lateral surface of sacrum (second to fourth vertebrae); exiting through the greater sciatic foramen; and inserting onto the superomedial greater trochanter. It neighbors with five hip rotator muscles: the superior and inferior gemelli, the obturator externus and internus, and the quadratus femoris. During lower extremity weight bearing or ambulation, the piriformis muscle contracts to prevent rapid internal rotation of the hip. It externally rotates the hip when the hip and knee are extended, whereas it abducts the hip when it is flexed to 90 degrees. The sciatic nerve, posterior femoral cutaneous nerve, gluteal nerves, and the gluteal vessels pass below the piriformis muscle. However, there are anatomic variations of the sciatic nerve to the piriformis muscle: superior to, divided by, or piercing through the piriformis muscle. There were numerous studies in the past in attempting to find out the cause of low back pain and sciatica. Yeoman dissected 100 cadavers to find the relationship of the sacroiliitis and sciatica.155 In 1934, Freiberg and Vinke assumed that the sacroiliac joint (SIJ) lesion caused inflammation in the piriformis muscle, its fascia, and the lumbosacral plexus leading to the irritation of sciatic nerve.156 Beaton and Anson related the anomalies of the piriformis muscle to sciatica.157 The term PS was first used by Robinson in 1947 when he described this syndrome with158 six cardinal features to describe this syndrome. The six key features are (1) a history of trauma or fall to the buttock; (2) gluteal or SIJ pain with radiation to the lower extremity; (3) gluteal atrophy; (4) a palpable sausageshaped mass; (5) positive Lasègue’s sign (pain on voluntary flexion, adduction, and internal rotation of the hip); and (6) exacerbation of pain with bending or lifting. The PS remains a controversial diagnosis as to whether it is a distinct clinical diagnosis of the tender piriformis muscle with the pathology of muscle spasms or hypertrophy, or the compression of the sciatic nerve by the piriformis muscle causing neuropathic pain; and is complicated with the pain from five neighboring short external rotators.159-161 However, the authors think that the two entities could be the manifestation of the same diagnosis with different stage or severity of the disorder. The incidence of PS ranges from 0.33% to 6%162-164 and accounts for 6% to 8% of the yearly cases of low back pain and sciatica in the United States.165 Patients with PS are typically 30 to 40 years old, female (three to six times more than their male counterparts)166-170 with a recent history of trauma to the buttocks or pelvis (usually from a fall), exacerbated activity intensity, or changes of low back, pelvis and lower extremity biomechanics due to lower extremity injuries, leg length discrepancy (≤0.5 inch), hip joint replacement, gait disturbances, even pregnancy.152,171-173 It is also seen more in long distance truck drivers, cyclists, tennis players, ballet dancers, and the like. The typical symptoms of PS include buttock pain with or without radiation to the ipsilateral lower extremity, to or below the knee. These symptoms may

be exacerbated with ipsilateral hip adduction, internal rotation or prolonged sitting (sitting intolerance), intercourse or bowel movement.157,162,169,172,174,175 Severe cases of PS may lead to gluteal atrophy,174,176 motor weakness of the S1 innervated muscles,168,169,176 foot drop,176,177 and sensory deficits.164,168,169,175,176 The diagnosis of PS was once thought to be a diagnosis of exclusion and because of the aforementioned symptoms, PS is very often misdiagnosed as sacroiliitis or lumbosacral radiculopathy.178 Therefore, careful evaluation to rule out the other causes is essential for the correct diagnosis and effective treatment. Patients with PS often have tenderness at the buttock region overlying the greater sciatic notch or the piriformis muscle or a taut muscle band (with or without trigger point) to palpation, with or without radiation to the ipsilateral lower radiation reproducing the patients’ symptoms.158,178 Several provocative maneuvers have been used to aid the diagnosis of PS, including the FADIR test (hip Flexion, ADduction and Internal Rotation, also known as FAIR, which is also a therapeutic position),97,169,179,180 the Pace test,162 the Freiberg test,156 and the Beatty test.166 Because the piriformis muscle is so deep, palpation of the muscle and the trigger point can be properly performed only by rectal or vaginal examination.162,174-176 Imaging studies, such as computed tomography (CT), ultrasound, or magnetic resonance imaging (MRI) are employed to rule out other potential sources of compression at or near the sciatic notch, such as intrapelvic abscess, occult tumor, or hematoma181-183 or in the lumbosacral spine. One helpful diagnostic aid is EMG. In the case of lumbosacral radiculopathy, the EMG examination may reveal abnormal spontaneous electrical activity in the lumbar paraspinal muscles, whereas in piriformis syndrome, no such abnormal electrical activity should be seen.184 Because the site of nerve compression is distal to the nerve root,185 other investigators have reported that H-wave studies are delayed when comparing the patient’s extended painful leg to the same leg in a position of adduction, internal rotation, and flexion.186 Conduction may be delayed when the muscle is at its thickest in the shortened position. The injury to the piriformis muscle may lead to the inflammation and muscle spasms, and the irritation of the sciatic nerve.162,187 Histamine, serotonin, prostaglandin, and bradykinin from the inflammation may irritate the sciatic nerve resulting in a cycle of pain, spasms, inflammation, and irritation.188,189 The characteristic signs and symptoms are sometimes caused by pain referred from piriformis MTrPs153,185,190,191 and sometimes are caused by compression of the sciatic nerve between the bony rim of the sciatic foramen and a hypertrophied piriformis muscle.192 Pace and Nagle suggested that focal irritation of the piriformis muscle leads to myofascial pain syndrome that can be treated with trigger point injec­tion.162 The nodular MTrP and its taut band can provide the increased muscle bulk and tension. Pain in these patients may come from the nerve entrapment and the referred pain from the piriformis MTrPs. An additional source of pain in these patients is the tendency for compression of motor nerves to activate MTrPs in the muscles supplied by that nerve. Although some clinicians think that this diagnosis is controversial, numerous peer-reviewed articles clearly define clinical, anatomic, and electrophysiologic evidence for this distinct condition causing low back and leg pain.152-154,180,186,193-195 The attachment of the muscle at the greater trochanter is prone to be equally involved and tender and is readily available for palpation. It is very useful to identify the central TrP tenderness in the region of the mid-belly as well as the attachment tenderness at both ends. This strengthens the MTrP diagnosis considerably. Contraction of muscles with MTrPs appears to be most painful when the

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muscle is voluntarily contracted in the shortened position. If the enthesopathy is sensitive enough, the muscle hurts when forcefully loaded in any position but particularly in the shortened position.

Treatment of Piriformis Syndrome with Botulinum Toxin In most cases, the conservative treatments, such as physical therapy with piriformis muscle stretching, NSAIDs, muscle relaxants, ultrasound, vapo-coolant spray coupled with soft tissue stretching, are effective in reducing the inflammation, spasms, and pain.152,153,164,172,174 It is also reported that repeated piriformis muscle injections with clonidine and bupivacaine provide long-lasting pain relief in patients with PS.196 For patients who failed to improve with conservative treatments, local injections of anesthetics and/ or corticosteroids may be considered and has been shown to be effective.186 However, some patients may gain short-term benefits from local MTrP injections but remain refractory to other treatment for long-term pain control. This subset of patients has demonstrated clear benefit from botulinum toxin treatment, especially if the piriformis muscle shows EMG evidence of involuntary muscle contraction.165,197-202 Porta conducted a comparative trial of botulinum toxin type A and methylprednisolone in group of 40 subjects included 23  patients with piriformis syndrome.146 Subjects were randomized to receive methylprednisolone or botulinum toxin type A (100  units). The 23  patients received injections in the piriformis muscle. At 60 days, the botulinum toxin group demonstrated statistically significant pain reductions as determined by their visual analog pain scale scores (P <0.0001). In addition, a trend was noted at 30 days post-injection with the botulinum toxin group having lower pain scores but this did not reach statistical significance. The exact benefit derived from the piriformis muscle injection is uncertain because the data was not subanalyzed by the muscle injected.146 Childers and colleagues199 conducted one of the earliest studies to examine the effectiveness of intramuscular botulinum toxin injections as a treatment for piriformis muscle syndrome. The authors examined a convenient sample of three consecutive patients. All patients presented with findings consistent with a diagnosis of piriformis syndrome and all had failed a trial of conservative management including NSAIDs, stretching, ultrasound, and piriformis trigger point injections.197 H-reflexes and segmental nerve conduction studies in all patients confirmed conduction block along the sciatic nerve above the gluteal fold, consistent with the diagnosis.186,203 The involved piriformis muscle in each patient was injected under fluoroscopic guidance with 100 units of botulinum toxin type A reconstituted in 5 mL of preservative-free saline.197 Pain reduction was assessed through pretreatment to post-treatment differences on a patient self-reporting instrument that recorded visual analog pain scale scores of pain intensity, psychological distress from pain, spasm frequency, and interference with daily activities. Results of this open label case series demonstrated that the average pain scores decreased from 6.1 to 3.4 and were 3.6 two weeks later.197 Twelve weeks later, two out of three patients had returned to their previous pain levels, whereas one patient sustained longer lasting benefit.197 The same author was the first to report a randomized, double-blind, placebo-controlled crossover trial of the effectiveness of botulinum toxin type A injections for refractory piriformis syndrome.198 Ten women initially enrolled and nine women completed the study. The subjects were randomized to receive either 100 units of botulinum toxin injection or saline under

the guidance of fluoroscopy or EMG.198 The primary outcome measure of interest was differences between the pre-injection and postinjection visual analog pain scale scores (VAS). After injection with the vehicle, decreases were detected, but only in one of the four categories (distress), in contrast to the botulinum toxin group in which decreases were observed under all VAS categories.198 In 2002, Fishman and colleagues evaluated the efficacy of botulinum toxin type A used in conjunction with physical therapy for piriformis syndrome in 67 subjects.165 The results in this doubleblind, placebo-controlled trial were measured on the visual analog scale. The patients injected with botulinum toxin experienced more relief from pain than the subjects receiving placebo (P = .001) and more relief than patients receiving lidocaine with steroid (P < .05).165 Yoon and colleagues conducted a prospective, single site, open label trial to evaluate the efficacy of botulinum toxin type A (150 units) in patients with piriformis syndrome resistant to conventional therapy.202 Twenty patients had botulinum toxin injected using CT guidance and nine patients served as active controls receiving an injection of dexamethasone (5 mg) and 1% lidocaine. Pain intensity scores, using a numeric rating system, were significantly lower at 4, 8, and 12 weeks after treatment than at baseline (P < .0001).202 Fishman and coworkers performed the first dose finding study for botulinum toxin type B in a cohort of eight consecutive patients receiving injections with 5000, 7500, 10,000 or 12,500 units.201 Visual analog pain scale scores were assessed at 0, 2, 4, 8, and 12 weeks.200 The subjects receiving the 12,500 units of botulinum toxin type B had the greatest clinical improvement at 3 weeks postinjection but then regressed over the following 5 weeks.200 Lang conducted a single center, open label study to evaluate the clinical safety and efficacy of botulinum toxin type B in patients with piriformis syndrome in 2004.201 Twenty patients were enrolled in the study and the injections were performed under electromyographic guidance with 5000 units of botulinum toxin type B. The study did not have controls and the single examiner was not blinded. Significant reductions in mean visual analog scale scores for buttock and hip pain were noted at 4, 12, and 16 weeks and low back pain at weeks 2, 12, and 16. When injecting myofascial trigger points in the piriformis muscle, it is difficult to localize accurately in such a deep muscle and the trigger points are located in the end-plate zone in the midbelly region of the muscle. In this case, use of EMG guidance to inject the neurotoxin specifically where end-plate potentials are observed will ensure optimal placement of the product.198 Because all or part of the sciatic nerve may occasionally traverse this part of the muscle, this use of EMG guidance is of additional importance. The local anesthetic, corticosteroid, and botulinum toxin injections in the aforementioned reports165,197-202 were all performed under some sort of guidance, including EMG, ultrasound, fluoroscopy, and CT. Additional studies also demonstrated the convenience, accuracy, and efficacy in the injection of piriformis muscle.204-207 Therefore, the authors strongly recommend that the piriformis injection therapy should be conducted under the guidance of one of the proven methods to ensure the safety, accuracy, and efficacy. Although there are associated disadvantages such as radiation exposure, contrast reaction, and increased cost, guided piriformis injections are widely used to ensure accurate placement of the medications and to avoid nerve injury around the piriformis muscle. After cadaver study, Benzon and colleagues208 used the lower border of the SIJ as their reference for the steroid injection

Botulinum Toxin Injections in Myofascial Pain Disorders  105

to the piriformis muscle and near the sciatic nerve for better symptom relief. They inserted the needle 2 cm lateral and 1 cm caudal to the SIJ—guided with a fluoroscopy while patients were prone. The insulated needle was advance until a motor response was elicited in the foot with a nerve stimulator. The needle was then withdrawn until the elicited motor response disappeared and the steroid was injected near the sciatic nerve. The needle was then further pulled back to the piriformis muscle belly, confirmed with contrast (Fig. 14-1), and followed with steroid injection to the muscle. Similar technique was reported by Betts209 and confirmed with a cadaver study.207 In a 10-year study of the diagnosis, treatment, and outcome of the PS, Fishman and colleagues210 inserted the needle at a point one third the distance from the greater trochanter to the area of maximum tenderness in the buttock at the depth of approximately 3 to 5 cm. Electromyographic localization of the piriformis muscle was conducted only when the location or depth of the needle placement was uncertain. We use a fluoroscopically guided technique published by one of the authors (MKC).198,211 The patient is placed in the prone position, the skin over the largest bulk of the buttocks is prepped and draped in a sterile fashion. The greater trochanter of the femur, the body of the sacrum, and the sciatic notch are identified using fluoroscopy. The skin is marked at the midway on a line that crosses the middle of the sciatic notch between the sacrum and the greater trochanter of the hip. A dual-purpose injection/electromyographic needle is inserted in an angle slightly lateral to medial until the ileum is encountered. It is then withdrawn slightly, and the injection site is visualized by fluoroscopy. To further verify the needle placement within the piriformis muscle, an electromyographic electrode is connected to the hub of the needle and a ground and reference electrode is secured to the lateral upper thigh. The patient is instructed to externally rotate the thigh to activate the piriformis muscle until brisk motor unit action potentials are observed.

Smith and coworkers212 reported in detail a technique of piriformis muscle injection with ultrasound guidance. The patient was placed in a prone position. The posterior superior iliac spine (PSIS) was palpated and scanned. The transducer was then placed horizontally across the PSIS, and then moved inferiorly while kept horizontally. The lateral sacrum was visualized medially and the posterior inferior iliac spine (PIIS) laterally. After the image was optimized, the following were observed “(1) medial: the lateral, hyperechoic bony margin of the sacrum; (2) superficial: hyperechoic skin, mixed echogenicity subcutaneous fat, and the hypoechoic marbled appearance of the overlying gluteus maximus; and (3) deep: the piriformis muscle appearing deep to the lateral sacral border (whereas the gluteus maximus is superficial to the sacrum), and traversing from cephalomedial to caudolateral beneath the gluteus maximus” (Fig. 14-2). The sciatic nerve was then identified, which was an oval, mixed-echogenicity structure lying superficial to the quadratus femoris and deep to the gluteus maximus (Fig. 14-3). After the sciatic nerve and its course and relationship with the piriformis muscle including the variation were verified, the piriformis muscle was

GMAX

PIR

A

Sacrum

GT ILIUM

RT PIR LG

Ilium

B Head of femur

Figure 14-1  Piriformis muscle and needle placement confirmation with ­contrast. (From Benzon HT, Katz JA, Benzon HA, Iqbal MS: Piriformis ­syndrome: Anatomic considerations, a new injection technique, and a review of the literature. Anesthesiology 98:1442-1448, 2003.)

Figure 14-2  Longitudinal ultrasound view of the piriformis muscle. A, “The piriformis (PIR) muscle-tendon is visualized as a thin, hyperechoic band passing medial (left) to lateral (right) toward the greater trochanter (GT). The piriformis travels deep to the gluteus maximus (GMAX) as it  passes out of the superior greater sciatic foramen, formed anteriorly by  the ilium. In this image, the lateral sacrum would lie just off-screen to the left.” B, “Transducer position is relative to skeletal landmarks to obtain ultrasound image shown in A. RT PIR LG, right piriformis, longitudinal view ­(parallel to the long axis of the muscle).”208 (From Smith J, Hurdle MF, Locketz AJ, ­Wisniewski SJ: ­Ultrasound-guided piriformis injection: Technique description and ­verification. Arch Phys Med Rehabil 87:1664-1667, 2006.)

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LAT

MED

SCN

ultrasound-guided techniques is evident in previous publications. Pitfalls may occur in cases using both techniques and are most likely operator dependent. Fanucci and coworkers199 used CT to guide their percutaneous botulinum toxin injection for PS treatment. With the success of delivering injectate to the piriformis muscle and significant PS symptom relief with the other techniques mentioned earlier, we do not recommend routine use of this technique to avoid unnecessary cost and radiation exposure to the patients.

QF

RT QF LG

ISCHIUM

Figure 14-3  Transverse ultrasound view of the sciatic nerve. “The transducer is placed in an anatomic transverse plane at the level of the distal-lateral aspect of the ischial tuberosity. Here, the conspicuity of the hyperechoic sciatic nerve is increased as it passes between the hypoechoic quadratus femoris (deep) and gluteus maximus (superficial). The nerve can then be traced cranially to visualize its passage deep to the piriformis.” LAT, Lateral; MED, Medial; QF, quadratus femoris; RT QF LG, Right side, ­quadratus femoris, ­longitudinal view (parallel to the long axis of the muscle); SCN, Sciatic nerve.”208 (From Smith J, Hurdle MF, Locketz AJ, Wisniewski SJ: ­Ultrasound-guided piriformis injection: Technique description and ­verification. Arch Phys Med Rehabil 87:1664-1667, 2006.)

again localized and the skin overlying the muscle was marked and prepared. Under ultrasound guidance, the needle was advanced medial to lateral, parallel to the long axis of the piriformis and the transducer, to the lateral sacrum. They stated that the operator can feel and visualize when the needle abuts the muscle sheath. The needle is then passed into the sheath or the muscle. In this process, the depth was controlled on the ultrasound image. The injectate in the piriformis muscle was collected as a bolus or tracked laterally between the multiple slips of the piriformis. The needle placement was also verified with contrast and real-time fluoroscopy. They indicated that this technique offers advantages compared to traditional imaging methods, “including accessibility, compact size, lack of ionizing radiation exposure, and direct visualization of neuromuscular structures”. Huerto and associates204 used a similar technique plus a motor stimulator for perisciatic and piriformis muscle injection and concluded that this technique is accurate, safe, and reproducible for piriformis injection. Reus and colleagues used the inferior gluteal artery as the landmark for localizing the sciatic nerve in their ultrasound-guided perisciatic steroid injection.205 The sciatic nerve was found slightly lateral to the inferior gluteal artery on the longitudinal section and the skin was marked and prepared. The direction of the needle was controlled by longitudinal section of the sciatic nerve. The piriformis muscle was not injected or mentioned in this technique. Using the technique by Smith and coworkers212 Finnoff and colleagues213 used a cadaveric model to claim that ultrasoundguided piriformis injections were significantly more accurate than fluoroscopically guided contrast-controlled injections. They indicated that despite the use of bony landmarks and contrast, most of the fluoroscopically attempted piriformis injections were placed superficially within the gluteus maximus. However, we think that more studies need to be conducted to support such a claim. Nevertheless, the success of using the fluoroscopy-guided and the

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146. Porta M. A comparative trial of botulinum toxin type A and methylprednisolone for the treatment of myofascial pain syndrome and pain from chronic muscle spasm. Pain. 2000;85:101-105. 147. Diaz JH, Gould HJ. Management of post-thoracotomy pseudoangina and myofascial pain with botulinum toxin. Anesthesiology. 1999;91: 877-879. 148. Lew HL, Lee EH, Castaneda A, et al. Therapeutic use of botulinum toxin type A in treating neck and upper-back pain of myofascial origin: A pilot study. Arch Phys Med Rehabil. 2008;89:75-80. 149. Ferrante FM, Bearn L, Rothrock R, King L. Evidence against trigger point injection technique for the treatment of cervicothoracic myofascial pain with botulinum toxin type A. Anesthesiology. 2005;103:377-383. 150. Abram SE. Does botulinum toxin have a role in the management of myofascial pain? Anesthesiology. 2005;103:223-224. 151. Foster L, Clapp L, Erickson M, Jabbari B. Botulinum toxin A and chronic low back pain: A randomized double-blind study. Neurology. 2001;56:1290-1293. 152. Hallin RP. Sciatic pain and the piriformis muscle. Postgrad Med. 1983;74:69-72. 153. Simons DG, Travell JG. Myofascial origins of low back pain. 3. Pelvic and lower extremity muscles. Postgrad Med. 1983;73:99-105. 154. Solheim LF, Siewers P, Paus B. The piriformis muscle syndrome. Sciatic nerve entrapment treated with section of the piriformis muscle. Acta Orthop Scand. 1981;52:73-75. 155. Yeoman W. The relation of arthritis of the sacroiliac joint to sciatica, with an analysis of 100 cases. Lancet. 1928;2:1119-1122. 156. Freiberg AH, Vinke TH. Sciatica and the sacroiliac joint. L Bone Joint Surg. 1934;16:126-136. 157. Beaton LE, Anson BJ. The sciatic nerve and the piriformis muscle: Their interrelation a possible cause of coccygodynia. J Bone Joint Surg Am. 1938;20:686-688. 158. Robinson DR. Pyriformis syndrome in relation to sciatic pain. Am J Surg. 1947;73:355-358. 159. Stewart JD. The piriformis syndrome is overdiagnosed. Muscle Nerve. 2003;27:644-646. 160. Fishman LM, Schaefer MP. The piriformis syndrome is underdiagnosed. Muscle Nerve. 2003;27:646-649. 161. Pećina M. Contribution to the etiological explanation of the piriformis syndrome. Acta Anat (Basel). 1979;105:181-187. 162. Pace JB, Nagle D. Piriformis syndrome. West J Med. 1976;124:435-439. 163. Bernard Jr TN, Kirkaldy-Willis WH. Recognizing specific characteristics of nonspecific low back pain. Clin Orthop Relat Res. 1987; 217: 266-280. 164. Parziale JR, Hudgins TH, Fishman LM. The piriformis syndrome. Am J Orthop. 1996;25:819-823. 165. Fishman LM, Anderson C, Rosner B. Botox and physical therapy in the treatment of piriformis syndrome. Am J Phys Med Rehabil. 2002;81:936-942. 166. Beatty RA. The piriformis muscle syndrome: A simple diagnostic maneuver. Neurosurgery. 1994;34:512-514. 167. Foster MR. Piriformis syndrome. Orthopedics. 2002;25:821-825. 168. Beauchesne RP, Schutzer SF. Myositis ossificans of the piriformis muscle: An unusual cause of piriformis syndrome. A case report. J Bone Joint Surg Am. 1997;79:906-910. 169. Benson ER, Schutzer SF. Posttraumatic piriformis syndrome: Diagnosis and results of operative treatment. J Bone Joint Surg Am. 1999;81: 941-949. 170. Bonica JJ. Definitions and taxonomy of pain. In: Bonica JJ, ed. The Management of Pain. Philadelphia: Lea & Febiger; 1990. 171. McCrory P, Bell S. Nerve entrapment syndromes as a cause of pain in the hip, groin and buttock. Sports Med. 1999;27:261–274. 172. Hughes SS, Goldstein MN, Hicks DG, Pellegrini Jr VD. Extrapelvic compression of the sciatic nerve. An unusual cause of pain about the hip: Report of five cases. J Bone Joint Surg Am. 1992;74:1553-1559. 173. Noftal F. The piriformis syndrome. Can J Surg. 1988;31:210. 174. Barton PM. Piriformis syndrome: A rational approach to management. Pain. 1991;47:345-352.

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110  Soft Tissue and Joint Injections 175. Hanania M, Kitain E. Perisciatic injection of steroid for the treatment of sciatica due to piriformis syndrome. Reg Anesth Pain Med. 1998;23:223-228. 176. Chen WS. Bipartite piriformis muscle: An unusual cause of sciatic nerve entrapment. Pain. 1994;58:269-272. 177. Carmody C, Prietto C. Entrapment of the sciatic nerve as a late sequela of injury to the hamstring muscles. A case report. J Bone Joint Surg Am. 1995;77:1100-1102. 178. Kirkaldy-Willis WH, Hill RJ. A more precise diagnosis for low-back pain. Spine. 1979;4:102-109. 179. Dobrusin R. An osteopathic approach to conservative management of thoracic outlet syndromes. J Am Osteopath Assoc. 1989;89:1046-1050. 180. Steiner C, Staubs C, Ganon M, et al. Piriformis syndrome: Pathogenesis, diagnosis, and treatment. J Am Osteopath Assoc. 1987;87:318-323. 181. Chen WS. Sciatica due to piriformis pyomyositis. Report of a case. J Bone Joint Surg Am. 1992;74:1546-1548. 182. Kinahan AM, Douglas MJ. Piriformis pyomyositis mimicking epidural abscess in a parturient. Can J Anaesth. 1995;42:240-245. 183. Ku A, Kern H, Lachman E, et al. Sciatic nerve impingement from piriformis hematoma due to prolonged labor. Muscle Nerve. 1995;18:789-790. 184. LaBan MM, Meerschaert JR, Taylor RS. Electromyographic evidence of inferior gluteal nerve compromise: An early representation of recurrent colorectal carcinoma. Arch Phys Med Rehabil. 1982;63:33-35. 185. Papadopoulos SM, McGillicuddy JE, Albers JW. Unusual cause of “piriformis muscle syndrome”. Arch Neurol. 1990;47:1144-1146. 186. Fishman LM, Zybert PA. Electrophysiologic evidence of piriformis syndrome. Arch Phys Med Rehabil. 1992;73:359-364. 187. Sayson SC, Ducey JP, Maybrey JB, et al. Sciatic entrapment neuropathy associated with an anomalous piriformis muscle. Pain. 1994;59:149-152. 188. Lynn B. Cutaneous hyperalgesia. Br Med Bull. 1977;33:103-108. 189. Jankiewicz JT, Hennrikus WL, Houkom JA. The appearance of the piriformis muscle in computed tomography and magnetic resonance imaging: A case report and review of the literature. Clin Orthop Rel Res. 1991;262:205-209. 190. Simons DG, Travell JG. Myofascial origins of low back pain. 1. Principles of diagnosis and treatment. Postgrad Med. 1983;73:66-70. 191. Simons DG, Travell JG. Myofascial origins of low back pain. 2. Torso muscles. Postgrad Med. 1983;73:81-92. 192. Chen WS, Wan YL. Sciatica caused by piriformis muscle syndrome: Report of two cases. J Formos Med Assoc. 1992;91:647-650. 193. Jankiewicz JJ, Hennrikus WL, Houkom JA. The appearance of the piriformis muscle syndrome in computed tomography and magnetic resonance imaging. A case report and review of the literature. Clin Orthop Rel Res. 1991;262:205-209. 194. Julsrud ME. Piriformis syndrome. J Am Podiatr Med Assoc. 1989; 79:128-131. 195. Noftal F. The piriformis syndrome. Can J Surg. 1988;31:210. 196. Naja Z, Al-Tannir M, El-Rajab M, et al. The effectiveness of clonidinebupivacaine repeated nerve stimulator-guided injection in piriformis syndrome. Clin J Pain. 2009;25:199-205.

197. Galate JF, Childers MK, Gnatz S. Effectiveness of botulinum toxin in refractory piriformis muscle syndrome [abstract]. Arch Phys Med Rehabil. 1997;78:1041. 198. Childers MK, Wilson DJ, Gnatz SM, et al. Botulinum toxin type A use in piriformis muscle syndrome: A pilot study. Am J Phys Med Rehabil. 2002;81(10):751-759. 199. Fanucci E, Masala S, Sodani G, et al. CT-guided injection of botulinic toxin for percutaneous therapy of piriformis muscle syndrome with preliminary MRI results about denervative process. Eur Radiol. 2001;11:2543-2548. 200. Fishman LM, Konnoth C, Rozner B. Botulinum neurotoxin type B and physical therapy in the treatment of piriformis syndrome: A dosefinding study. Am J Phys Med Rehabil. 2004;83:42-50. 201. Lang AM. Botulinum toxin type B in piriformis syndrome. Am J Phys Med Rehabil. 2004;83:198-202. 202. Yoon SJ, Ho J, Kang HY, et al. Low-dose botulinum toxin type A for the treatment of refractory piriformis syndrome. Pharmacotherapy. 2007;27:657-665. 203. Childers MK, Biswas SS, Petroski G, et al. Inhibitory casting decreases a vibratory inhibition index of the H-reflex in the spastic upper limb. Arch Phys Med Rehabil. 1999;80:714-716. 204. Huerto AP, Yeo SN, Ho KY. Piriformis muscle injection using ultrasonography and motor stimulation—report of a technique. Pain Physician. 2007;10:687-690. 205. Reus M, de Dios Berná J, Vázquez V, et al. Piriformis syndrome: A ­simple technique for US-guided infiltration of the perisciatic nerve. Preliminary results. Eur Radiol. 2008;18:616-620. 206. Spiller J. Acupuncture, ketamine and piriformis syndrome—a case report from palliative care. Acupunct Med. 2007;25:109-112. 207. Gonzalez P, Pepper M, Sullivan W, Akuthota V. Confirmation of needle placement within the piriformis muscle of a cadaveric specimen using anatomic landmarks and fluoroscopic guidance. Pain Physician. 2008;11:327-331. 208. Benzon HT, Katz JA, Benzon HA, Iqbal MS. Piriformis syndrome: anatomic considerations, a new injection technique, and a review of the literature. Anesthesiology. 2003;98:1442-1448. 209. Betts A. Combined fluoroscopic and nerve stimulator technique for injection of the piriformis muscle. Pain Physician. 2004;7:279-281. 210. Fishman LM, Dombi GW, Michaelsen C, et al. Piriformis syndrome: Diagnosis, treatment, and outcome—a 10-year study. Arch Phys Med Rehabil. 2002;83:295-301. 211. Childers MK, Kornegay JN, Aoki R, et al. Evaluating motor endplate-targeted injections of botulinum toxin type A in a canine model. Muscle Nerve. 1998;21:653-655. 212. Smith J, Hurdle MF, Locketz AJ, Wisniewski SJ. Ultrasound-guided piriformis injection: Technique description and verification. Arch Phys Med Rehabil. 2006;87:1664-1667. 213. Finnoff JT, Hurdle MF, Smith J. Accuracy of ultrasound-guided ­versus fluoroscopically guided contrast-controlled piriformis injections: a cadaveric study. J Ultrasound Med. 2008;27:1157-1163.

Prolotherapy: A CAM Therapy for Chronic Musculoskeletal Pain

15

David Rabago, MD, Jeffrey J. Patterson, DO, and Joel Jay Baumgartner, MD Prolotherapy is an injection-based complementary and alternative medicine (CAM) therapy for chronic musculoskeletal pain. The historical roots of therapeutic intervention that may have similar underlying mechanisms of action, however, extend to antiquity. Hippocrates anecdotally described the use of hot wires to create scar tissue (sclerotherapy, an early name for prolotherapy) in cases of severe shoulder dislocation in soldiers. Prolotherapy injections have been used for approximately 100 years by physicians practicing both conventional and complementary medicine. Modern applications can be traced to the 1950s when prolotherapy injection protocols were formalized by George Hackett,1 a general surgeon in the United States based on his clinical experience of more than  30 years. Although techniques and injected solutions vary by condition, clinical severity, and practitioner preferences, a core principle of contemporary prolotherapy is that a relatively small volume of an irritant or sclerosing solution is injected at sites on painful ligament and tendon insertions, and in adjacent joint space over the course of several treatment sessions.1,2 Prolotherapy is becoming increasingly popular in the United States and internationally, and is actively used in clinical practice.3,4 Increased quantity and quality of the scientific literature supporting prolotherapy, internet reports, and the use of prolotherapy by prominent sports personalities all contribute to a growing visibility and interest among physicians and patients. A 1993 survey sent to osteopathic physicians estimated that 95 practitioners in the United States were estimated to have performed prolotherapy on approximately 450,000 patients. However, this survey likely underestimated the true number of practitioners dramatically because only 27% of surveys were returned.5 No formal survey has been done since 1993. The current number of practitioners actively practicing prolotherapy is not known but is likely several thousand in the United States based on attendance at CME conferences and physician listings on relevant websites. Prolotherapy has been assessed as a treatment for a wide variety of painful chronic  musculoskeletal conditions that are refractory to “standard of care” therapies. Although anecdotal clinical success guides the use of prolotherapy for many conditions, clinical trial literature supporting evidence-based decision-making for the use of prolotherapy exists only for low back pain, several tendinopathies, and osteoarthritis.

Nomenclature Nomenclature surrounding prolotherapy has evolved. This procedure, now known most commonly as prolotherapy, has been identified using names consistent with existing hypotheses and

understanding of possible mechanisms of action. Nomenclature has reflected practitioners’ perceptions of prolotherapy’s therapeutic effects on tissue. Historically, this injection therapy was called “sclerotherapy” because early solutions were thought to be scar-forming. “Prolotherapy” is currently the most commonly used name, and is based on the presumed “proliferative” effects on chronically injured tissue. It has also been called “regenerative injection therapy” (RIT)2,6; some contemporary authors identify the therapy according to the injected solution.7 The precise mechanism of action of the various injectants is not known, but is likely to be multifactorial.

Professional Status No single national medical organization acts as a supervisory, credentialing, or guideline-generating capacity for prolotherapy or its practitioners. The National Institutes of Health identifies prolotherapy as a CAM therapy. The NIH National Center for Complementary and Alternative Medicine (NCCAM) has funded two ongoing clinical trials and two completed basic science studies on the mechanisms of prolotherapy.8,9 The Centers for Medicare and Medicaid Services and the Veteran’s Administration have reviewed the prolotherapy literature for low back pain and all musculoskeletal indications, respectively, and determined existing evidence to be inconclusive. Neither agency recommends third party compensation for prolotherapy. However, neither review included the most recent clinically positive studies or reviews in their evaluation.7,10-13 Private insurers are beginning to cover prolotherapy for selected indications and clinical circumstances; however, most patients pay “out-of-pocket”.

Prolotherapy Technique Like contemporary Western medical therapies, CAM therapies often follow directly from a particular way of understanding the patient’s normal and pathologic conditions. For example, acupuncture relies on an ancient tradition of energy meridians and physiologic correlations that inform the specific procedures of needle placement to improve overall balance. Meditation relies on an understanding of interaction between mind and body to influence the body using mental processes. The same is true of prolotherapy. In his clinical text on the practice of prolotherapy, George ­Hackett  laid out the foundations of treating musculoskeletal injuries  113

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using prolotherapy. He developed a diagnostic and treatment strategy familiar to those with a detailed knowledge of conventional ­Western understanding of the effects of local trauma, healing, and pain referral patterns. His diagnostic and therapeutic techniques, developed in the 1950s, could be viewed as holistic before the term gained popularity in contemporary medicine. Hackett interpretated chronic pain and referred pain symptoms such as numbness, tingling, and weakness, and alteration in proprioception, as originating, in part, from poorly healed ligaments and tendons. As such, he preceded by several decades the current change in the understanding of chronic tendon and ligament pain. Formerly thought to be primarily inflammatory in nature (“tendonitis), chronic tendon injury is now understood to be primarily a result of noninflammatory, degenerative tissue (tendinosis). Injection protocols for a particular body part tend to treat not just the specific injured structure, but also the surrounding structures, in an effort to increase the integrity of the area as a whole. During a prolotherapy session, therapeutic solutions are injected at sites of painful and tender ligament and tendon attachments, and into adjacent joint spaces. Prolotherapy treatment commonly consists of several injection sessions delivered every 2 to 6 weeks over the course of several months. Injections are often carried out in a joint-specific manner. The actual prolotherapy procedure can be illustrated using a specific clinical scenario as an example discussed subsequently. In this section we describe a standard set of injections of the anterior knee. Prolotherapy is commonly performed by prolotherapists for patients with knee osteoarthritis who have one or more areas of anterior knee area tender to palpation. Injections are carried out in a “peppering” fashion throughout the tender tendon or ligament attachments with all injections done with the needle touching bone. This description is intended to demonstrate the overall process and anatomic detail with which a prolotherapist approaches a specific condition. It is not intended as a substitute for formal prolotherapy training. Although there is no consensus regarding specific indications or procedural elements of prolotherapy, there is some consistency among prolotherapists concerning what constitutes appropriate injections of specific anatomic areas. The following example explains a set of injections for knee osteoarthritis and, in the authors’ view, can be viewed as a general approach for a majority of practicing prolotherapists.

Clinical Vignette Patient Description JM is a 55-year-old woman with knee pain for 3 years who is referred by her primary care physician for consideration of prolotherapy for knee osteoarthritis. Prior work-up revealed moderate joint space narrowing on plain radiograph. The patient denies prior knee trauma. Her knee pain worsens with activity but her knee does not “give out” or “lock”. Prior therapy has included rest, acetaminophen, and nonsteroidal antiinflammatory drugs (NSAIDs). Her examination reveals a noninflamed knee with crepitus on flexion and extension but without effusion. The knee is stable with near-normal range of motion and normal Lachman’s test. There is moderate tenderness to palpation of the pes anserine muscle group insertion, the medial popliteal attachments, and the proximal attachment of the medial collateral ligament. Approach to the patient: Routine office evaluation has determined that the patient has moderate knee osteoarthritis and

anterior knee pain without meniscal injury, posterior or anterior cruciate ligament injury, or other surgical issues. She seems to be a good candidate for prolotherapy. The overall clinical situation is discussed with the patient. She elects to proceed with a trial of prolotherapy. Position: The patient may be positioned with the knee flexed at 90 degrees or extended while lying prone at 180 degrees.  The flexed position is preferred because it is somewhat easier to inject relevant structures with the patient’s leg relaxed and leaning against the injector, and it allows better access to anterior knee structures. Anatomic marking and local anesthesia: The major superficial anatomic landmarks are palpated and marked with skin marker of choice (Fig. 15-1). Tender areas are injected with small intradermal skin wheals because this makes the deeper injections less ­painful. One percent buffered lidocaine is often used.

Injection of Ligamentous and Tendinous Attachments Injections are performed through the skin wheal with the needle tip on bone with solution delivered in a peppering fashion approximately each square centimeter. A single skin puncture can be used to facilitate multiple placements of solution. After the initial needle positioning, the needle is either: (1) lifted slightly from the surface of the bone and repositioned, or (2) the skin is slid (skin sliding). Between 0.2 to 0.5 mL of solution is placed at each location. The order of injected anatomic sites injected is clinician-specific. The following order is used in the authors’ clinic. 1. M  edial knee: Injections begin at the superior aspect of the femoral condyle along the femur distally to the joint line. Injections are then made at the anterior tibia and the attachments of the pes anserine tendons. It is likely that these structures and not the much smaller bursa is the source of pain in this area. The popliteus muscle attachment is injected by displacing the medial calf musculature posteriorly; injections are done by directing the needle anteriorly onto the posterior tibia. Injections are then made on the joint line directed downward onto the top of tibia into attachments of the coronary ligaments, which attach the medial meniscus to the tibia. The patella is injected at the superior and inferior lateral and medial retinaculum. 2. L  ateral knee: The superior condyle of the femur is the first structure of the lateral knee to be injected. It is followed by the lateral collateral ligament, lateral joint line, and lateral coronary ligaments. The fibula is then palpated with thumb and forefinger over the head of fibula, and injections are done to top and anterior edge of the fibula and into tibiofibular ligament at the anterior portion of fibula.

3. I ntra-articular knee injection: An intra-articular injection is often performed as part of an anterior knee injection series; the most common access is the anteromedial port. The actual injection is consistent with that of a routine intra-articular steroid injection. Alterative access includes the lateral superior port, which can be palpated with the knee straight, and is located at the lateral patella, approximately 1 cm below the superior edge of the patella. Intra-articular access can be improved by applying pressure to the medial side of the patella and lifting its lateral border superiorly, thereby creating a wider port of entry  (Fig. 15-2).

Prolotherapy: A CAM Therapy for Chronic Musculoskeletal Pain  115

15 5

1. Medial collateral ligament (broad attachments to femur and tibia)

6

2. Pes anserine 3. Tibial tuberosity

1

7

5

6

4

4. Coronary ligaments (stabilizes meniscus)

2

3

5. Patella

4

6. Lateral collateral ligament 7. Access intra-articular space

Medial view

Lateral view

Figure 15-1  Medial and lateral views of knee marked prior to placement of skin wheals and prolotherapy injections.

5 1 6 1. Medial collateral ligament (broad attachments to femur and tibia) 2. Pes anserine 3. Tibial tuberosity 4. Coronary ligaments (stabilizes meniscus)

5 6

6 1

4

7

4

5

5. Patella 6. Lateral collateral ligament 7. Intra-articular injection

2

1

3

Figure 15-2  Anatomic locations for prolotherapy injections at the anterior knee. (Knee image courtesy Primal Pictures Ltd. www.primalpictures.com. Used by permission.)

116  Complementary and Alternative Medical Procedures

Mechanism of Action Injected solutions (“proliferants”) have historically been hypothesized to cause local irritation, with subsequent inflammation and tissue healing resulting in enlargement and strengthening of damaged ligamentous, tendinous, and intra-articular structures.14,15 These processes were thought to improve joint stability, biomechanics, function, and ultimately, to decrease pain.1,2 The mechanism of action for prolotherapy is not clearly understood and, until recently, it received little attention. Supported by pilot-level evidence, the three most commonly used prolotherapy solutions have been hypothesized to act via different pathways: hypertonic dextrose by osmotic rupture of local cells, phenolglycerine-glucose (P2G) by local cellular irritation, and morrhuate sodium by chemotactic attraction of inflammatory mediators16 and sclerosing of pathologic neovascularity associated with  tendinopathy.17,18 The potential of prolotherapy to stimulate release of growth factors favoring soft tissue healing has also been suggested as a ­possible mechanism.19,20 In vitro and animal model data have not fully corroborated these hypotheses. An inflammatory response in a rat knee ligament model has been reported for each solution, although this response was not significantly different from that caused by needle stick alone or saline injections.8 However, animal model data suggest a significant biologic effect of morrhuate sodium and dextrose solutions compared to controls. Rabbit medial collateral ligaments injected with morrhuate sodium were significantly stronger (31%), larger (47%), and thicker (28%), and had a larger collagen fiber diameter (56%) than saline-injected controls14; an increase in cell number, water content, ground substance amount, and a variety of inflammatory cell types were hypothesized to account for these changes.15 Rat patellar tendons injected with morrhuate sodium were able to withstand a mean maximal load of 136% (±28%)—significantly more than the uninjected control tendon.21 Interestingly, in the same study, tendons injected with saline control solution were significantly weaker than uninjected controls.21 Dextrose has been minimally assessed in animal models. Recent studies showed that injured medial collateral rat ligaments injected with 15% dextrose had a significantly larger cross-sectional area compared to both noninjured and injured saline-injected controls.22 P2G solution has received the least research attention; although it is in active clinical use, no animal or in vitro study has assessed P2G effect using an injury model. In research settings, most clinicians report using these solutions as single agents, although concentration of each one varies. In clinical practice, physicians sometimes mix prolotherapy solutions, or use solutions serially in a single injection session depending on experience and local practice patterns. The effect of varied concentrations or mixtures has not been assessed in basic science or clinical studies and no clinical trial has compared various solutions.

Clinical Evidence Early Research Since its inception, prolotherapy has been primarily performed outside of academia. Research has been primarily done by clinicians who perform prolotherapy themselves. This has lead to a

pragmatic orientation of existing prolotherapy studies and a relative paucity of large, rigorous, clinical trials in spite of significant clinical activity. Although the first randomized controlled trial (RCT) did not appear until 1987, clinicians have enthusiastically reported the results of more modest, pilot-level nonrandomized clinical trials since the 1930s (Tables 15-1 and 15-2). In 2005, our group reported the results of a systematic review of prolotherapy for all indications; we found 42 published reports of clincal prolotherapy trials since 1937.23 Thirty-six of the studies to date were case reports and case series that included 3928 patients aged 12 to 88 years. These uncontrolled studies provide the earliest and most clinically-oriented evidence for prolotherapy. Each study reported positive findings for patients with chronic, painful, refractory conditions. Report quality of the included studies varied widely; their internal methodologic strength was generally consistent with publication date. The older case studies documented several injectants and methods that are no longer in use. Contemporary solutions were noted to start with P2G in the 1960s, dextrose in the 1980s, and morrhuate sodium in the early 1990s. The case reports and case series highlighted the fact that, over time, prolotherapy has been used and studied for a continually growing set of clinical indications. These case studies have also been used as pilots to develop new assessment techniques that could help elucidate pathophysiology of the condition in question7 and test methodology for future, more robust randomized trials.24 In general, while lacking control groups and randomization, these pragmatic studies25 had the advantage of assessing effectiveness of prolotherapy in “real life settings” that patients encounter, including the prolotherapist’s ability to select the patient and to individually tailor the injection protocol. Most of the subjects (72%, 2691 of 3741) assessed in the early literature were treated for low back pain. However, other indications assessed by these early studies included knee osteoarthritis, shoulder dislocation, neck strain, costochondritis, lateral epicondylosis and other tendinopathies, and fibromyalgia (see Tables 15-1 and 15-2).

Contemporary Research Research on prolotherapy and its clinical effects has accelerated, and the number and methodologic quality of studies assessing prolotherapy have increased dramatically since the mid-1980s (Fig. 15-3). To date, prolotherapy has been evaluated using moderateto-strong assessment techniques and study designs as a treatment for low back pain, osteoarthritis, and several tendinopathies; each condition is a significant cause of pain and disability, and is often refractory to best standard-of-care therapies. The societal impact of these conditions will likely increase in the coming years because the severity and prevalence of each condition is age related. Because the United States population is aging, finding new effective therapies for these conditions can have an impact on individual patient care and overall public health. If effective, the import of nonsurgical interventions such as prolotherapy will also grow. The following section gives an integrated description of higher quality studies assessing prolotherapy for these clinical indications, presented in an order of descending strength of evidence; RCTs are described first (see Table 15-3), and scored using the Delphi scoring system.26 A summary table follows that assigns a formal level of evidence grade for prolotherapy for each condition (Table 15-4).

Table 15-1  Description of Case Reports and Case Series Indication

Subjects

Injectant

Outcome Measures

Results

Gedney et al., 193787

Knee OA pain, knee insta­ bility, LBP, SI dysfunction

1 F, age 68 yrs; 1 M, age 45 yrs

Neoplasmoid* and MacDonald’s Solution* injection

Subjective pain and mobility

Improved mobility, decreased pain

Shuman et al., 194188

Recurrent shoulder dislocation

1 F, age 23 yrs; 3 M, ages 17, 18, 24 yrs

AC joint capsule injections using one or more of the following: Sodium Linsoleate*, Alparene*, Sylnasol*, Neoplasmoid*

Subjective pain, recurrence of dislocation

No recurrence of dislocation, decreased pain

Bahme et al., 194589

SI dysfunction

30 F, 70 M; ages 12-75 yrs; pain for 0.5-45 yrs

OM and SI ligament Sylnasol* injections

Subjective pain

50%-100% pain relief

Gedney et al., 195190

LBP

3 M, ages 19, 32, 34; pain for 0.5-16 yrs

Sylnasol* injections

Work status, subjective pain

Ability to return to work, decreased pain

Gedney et al., 195291

SI dysfunction, LBP

1 F, age 23 yrs; 1 M, age 30 yrs; pain for 1 yr

SI ligament Sylnasol* injections

Subjective pain

Resolution of pain

Hackett et al., 195392

SI dysfunction, LBP

9 M, 8 F; ages 15-52 yrs; pain for 4 mos-20 yrs

Sylnasol* injections

Subjective pain

Resolution of pain through 2 yr follow-up Occasional exacerbation resolved with retreatment

Hackett et al., 195392

SI dysfunction

119 M , 134 F; ages 15 to 70; pain for up to 30 yrs

Not given

Subjective pain

Pain-free for 2-14 yrs (long-term followup questionnaire)

Shuman et al., 195493

LBP, knee pain, shoulder separation, other joint pain

93 adults

Not given

Return to work

95% (88) able to return to work, 5% (5) unable to return to work

Hackett et al., 195494

SI dysfunction

3 F, ages 40, 56, and 58 yrs

Not given

Subjective pain

Resolution of pain

Neff et al., 196095

LBP, SI dysfunction

3 adults

Sylnasol* injections

Subjective pain

Resolution of pain

Myers et al., 196196

LBP

267 adults

Sylnasol/pontocaine* solution or Zinc/phenol* solution injections

Subjective pain

Resolution of pain in 82% of subjects

Hackett et al., 196297

SI dysfunction, other joint pain

1857 subjects (1516: SI dysfunc­ tion, 284: other indications); ages 15-88 yrs; pain/disability for 3 mos to 65 yrs

Sylnasol* or P2G injections

Subjective pain

“Satisfactory cure” in 82% (1489) ­subjects for up to 19 yrs

Hackett et al., 196297

Head-neck strain

82 subjects

P2G injections

Subjective pain

“Good to excellent” results in 74 subjects

Kayfetz et al., 196398

Traumatic (whiplash) or nontraumatic (tension) headache

102 M, 162 F subjects (206 traumatic, 58 nontraumatic headache); pain (average) for 4 yrs

Sylnasol*, zinc sulfate* or P2G5 injected during 1-20 sessions

4-point pain scale: from excel­ lent (no pain or symptoms) to poor (no relief of pain or symptoms)

Pain improvement during 6 mos to 5 yrs follow-up: excellent: 145; good: 43; fair: 41; poor: 33; lost to follow-up: 2 Continued

Prolotherapy: A CAM Therapy for Chronic Musculoskeletal Pain  117

Study

15

Study

Indication

Subjects

Injectant psylliate*,

Outcome Measures

Results

Kayfetz et al., 196399

Occipitocervical injury (whiplash)

87 M, 102 F; ages 10-61 yrs; pain for >1 mo in 78%, pain for >1 yr in 21% of subjects

Sodium tetradecyl sulfate*, zinc sulfate* injected in 1-20 sessions over 1 to 6 mos

4-item pain scale: from excel­ lent (no pain or symptoms) to poor (no relief of pain or symptoms)

Pain improvement: excellent: 113; good: 15; fair: 34; poor: 27

Peterson et al., 1963100

LBP

136 adults

P2G injections

Pain improvement (percentage of improvement)

Pain improvement: excellent (>75%): 106; good (50-75%): 114; fair (25-50%): 5; poor (<25%): 11

Barbor et al., 1964101

LBP

153 adults; pain for 6 mos-20 yrs

P2G injections

Subjective pain relief

Pain relieved to subject’s   satisfaction: 111; Pain relief failure: 17; Lost to follow-up: 25

Blumenthal et al., 1974102

Headache

3 adults

P2G injections

Subjective pain

Resolution of pain

Leedy et al., 1976103

LBP

50 adults; ages 25-72 yrs; pain for 1 mo to >10 yrs

Not given

Subjective pain at 5-yr follow-up

Pain resolution with: 0 exacerbation: 26 1 exacerbation: 18 2 exacerbations: 5 >2 exacerbations: 1

Leedy et al., 1977104

Shoulder pain, LBP, costo­ chondritis, epicondylitis

4 M, 4 F

Farnsworth formula 61* injections

Subjective pain

Symptom resolution

Leedy et al., 1982105

SI dysfunction

4 M, 18-55 yrs; 1F, 82 yrs

Not given

Subjective pain

Symptom relief

Bourdeau et al., 1988106

LBP

11 M, 13 F; ages 19-82 yrs; pain for 2 mos to 30 yrs

12.5% dextrose injections in 3-10 treatment sessions

4-point pain scale at 5-yr follow-up

Excellent (little or no pain for 5 yrs): 7; Very good (little or no pain for   2-5 yrs): 10; Good (little or no pain for 1 yr): 2; Poor (pain control for less than 6 mos): 5

Ongley et al., 1988107

Knee pain, knee laxity

4 subjects

30-40 mL P2G “peppered” into PCL, ACL, LCL, MCL insertions

Laxity measured with “Genucom” knee analysis system; subjective pain and function

Improvement for 90° A-Ph draw, 90° A-P draw with internal rotation, 30° A-P draw, and 80° internal-external rotation (P < .05); Complete pain resolution: 2 Partial pain improvement: 2 Function improvement: 4

LaCourse, et al., 1990108

LBP

8 adults

P2G injections; subjects also received lidocaine and steroid injection, and exercise advice

Pelvic inclination as measured by inclinometer

Decreased pelvic inclination

Dorman, et al., 1991109

Low-back, mid-back and neck pain

40 F, 40 M adults

P2G injections; subjects also received lidocaine and steroid injection, and exercise advice

Pain severity, functional capacity, sleep

Decreased pain severity, improved functional status and sleep

Schwartz et al., 1991110

SI dysfunction

43 adults; ages 20-70 yrs

3 injections with SM each 2 weeks apart

Pain relief scale at 2-week follow-up

Pain relief: 95%: 20; 75%: 11; 66%: 4; 33%: 1; 0%: 3

118  Complementary and Alternative Medical Procedures

Table 15-1  Description of Case Reports and Case Series—cont’d

Iliocostal friction syndrome

6 M, 6 F; ages 38-82 yrs

12.5-25% dextrose injections and use of rib compression belt and Hoek corset

Subjective pain

Resolution of pain

Reeves et al., 1994112

Fibromyalgia

31 adults; pain (average) for 7-8 yrs

12.5% dextrose injected at 16 fibromyalgia sites an average of 3.5 times

Average pain (0-10 Likert scale); subjective functional status

Average pain improvement of 16%; Improved functional status

Dorman et al., 1995113

LBP

9 adults

Proliferant and protocol not given

Oxygen consumption efficiency while walking

Improved oxygen consumption efficiency while walking

Mathews, 1990114

SI dysfunction

16 subjects

3 series of P2G injections

5-item pain scale

At 4-mos follow-up: no pain: 11; slight pain: 1; much better: 1; slightly better: 1; no better: 1; Lost to follow-up: 1

Reeves et al., 1997115

Recurrent knee dislocation

1 F, age 72 yrs

5% dextrose injections

Subjective pain; dislocation

Decreased pain Joint relocation

Reeves et al., 2003116

Knee pain, flexion and laxity

16 adults

10% and 25% dextrose injections

Pain scale; knee laxity

At 3-yr follow-up: pain at rest, stair, and walk decreased by 35-45%; subjective swelling (P < .05) and ROM (P < .01) improved, ligament laxity decreased by 71% (P < .01).

Hooper et al., 2004117

Cervical, thoracic and lumbar pain

126 F, 51 M subjects; average age 39.5 yrs; pain for 3 mos-27 yrs (average: 4.8 yrs)

20% dextrose injections; weekly set of injections for 3 sessions with repeated set of 3 sessions if pain control incomplete

Subjective pain, function and ability to work on three 5-item scales

At mean 9 mos follow-up: Pain reduction: 91% of subjects; function improvement: 84.8% of subjects; improved ability to work (for those work­ ing outside the home): 84% of subjects

Hooper et al., 2005118

Cervical pain

1 M subject; neck pain (MVA-related) for 2 yrs

Intra-articular 20% dextrose   injected under fluoroscopic guid­ ance at zygapophyseal joints C2-C6

Neck disability index score (NDI)

NDI score decreased from 24/50 prein­ jection to 9/50 at 1 yr, and 2/50 at 3 yrs

Lazzara et al., 2005119

Full-thickness Achilles tendon rupture

1 F, 26 yrs; pain and inability to bear weight; MRI proven right Achilles tendon rupture 4.3 cm proximal to the calcaneus and 1.1 cm gap

Injections of 20 mL solution (SM, dextrose, 2% lidocaine and bacteriostatic water) at the Achilles tendon, anterior talofibular and calcaneofibular ligaments, and ankle joint biweekly for 8 sessions over 3 mos

Subjective pain, disability, ultrasound and MRI

No subjective pain at rest or while jog­ ging and has normal gait. MRI showed no defect at 10 weeks, ultrasound at 14 weeks showed tendon significantly larger than unaffected side

Topol et al., 200547

Groin pain (osteitis pubis and/or adductor tendinopathy)

24 M rugby and soccer players pain (average) for 15.5 mos

12.5% dextrose injected at the pubis symphysis and ischiopubic ramus at 4-week intervals for 2-6 injection sessions (mean 2.8)

VAS, Nirschl Pain Phase Scale

Improvement in both outcome measures (P < .05); 22/24 subjects plying at full capacity at mean 17 mos follow-up   (6 to 32 mos)

Maxwell et al., 20077

Achilles tendinopathy (insertional and midportion)

11 F, 25 M adults ages 23-82 yrs (mean: 52.6 yrs); pain for 3 mos-120 mos (average: 28.6 mos)

25% dextrose injected into anechoic and hypoechoic areas of the tendon every 6 weeks for mean of 4 sessions (2-11)

100 mm VAS for pain at rest, with activity and during sport; tendon thickness; degree of neovascularity, hypoecho­ genicity

Sustained at 12 mos follow-up: VAS pain at rest: 81% improvement; VAS pain with activity: 84% improvement; VAS pain during sport: 78% improvement; Decrease in tendon thickness, hypoecho­ genicity and neovascularity. Continued

Prolotherapy: A CAM Therapy for Chronic Musculoskeletal Pain  119

Hirschberg et al., 1992111

15

Study

Indication

Subjects

Injectant

Outcome Measures

Results

Miller et al., 200665

Chronic degenerative discogenic leg pain

35 F, 41 M ages 21-90 yrs (mean 55 yrs) with pain for 2-240 (mean 39 mos) who failed physical therapy; had substantial but temporary relief with two fluoroscopically guided epidural steroid injections and had CT-proven multiple grade IV or V tears of the annulus fibrosis

3 mL 25% dextrose; biweekly disc space injection for mean of 3.5 injection sessions

0-10 VAS pain scale

43.4% of subjects had sustained improve­ ment with a mean of 71% improvement at mean follow-up of 18 mos compared to baseline status. 43.4% (33/76) of subjects showed a sustained treatment response of 71% Baseline VAS for responders was 8.9 (±1.4), 2.5 (±2.0) at 2 mos, and 2.6 (±2.2) at 18 mos

Khan, et al., 200863

Refractory coccygodynia

23 F, 14 M adults (mean 36 yrs) with > 6 mos of pain

25% dextrose injected to tender coccyx points in 1-3 injections depending on initial pain level.

0-10 VAS pain scale

At 2 mos, reduction of VAS from 8.5 at baseline to 2.5. 30/37 achieved “good” pain improvement; 7/30 “not improved”.

Cusi et al., 200862

SI joint pain with failure of load transfer (disability) at the SI joint

20 F, 5 M adults ages 26-67 (mean 40.4 yrs); at least 6 mos of LBP who failed 3 mos PT

Computer tomography-guided injection of (1.8 mL/5 mL 50% dextrose to dorsal interosseous ligament each 6 weeks for 3 sessions and continued to perform PT program

Quebec Back Pain Scale, Roland Morris 24, Roland Mor­ ris Disability Scale

At 26 mos average (range 6-39 mos): Improvement compared to baseline status in all pain and disability measures (P < .01)

Ryan et al., 200812

Plantar fasciitis

17 F, 3 M adults mean age 51   (SD 13) yrs; at least 6 mos of symptoms of plantar fasciitis who failed one or more conservative treatments

Ultrasound-guided injection of 25% dextrose with lidocaine; abnormal hypoechoic areas and anechoic clefts/foci in the thickened portion of the plantar fascia were targeted

0-100 VAS pain levels and percentage pain reduction at rest, activities of daily living, and activity Ultrasound assessed tendon thickness, number of tendons with anechoic clefts or foci, and degree of neovascularity

At 12 mos follow-up, subjects reported a mean change on VAS of 12.1 (21.0), 21.6 (29.5), and 35.1 (41.4) points at rest, activities of daily living, and physical activity, respectively They also reported pain reduction of 88%, 84%, and 78% at rest, activities of daily living, and physical activity Structurally, there was a mean reduction in tendon thickness, number of tendons with anechoic clefts or foci, and degree of neovascularity

*No

longer used for prolotherapy or no longer available. ACL, Anterior cruciate ligament; A-P, Anterior-posterior; LBP, Low back pain; LCL, Lateral collateral ligament; MCL, Medial collateral ligament; mos, Months; OA, Osteoarthritis; OM, Osteopathic manipulation; P2G, Phenol-glucose-glycerine; PCL, Posterior cruciate ligament; SI, Sacroiliac; SM, Sodium morrhuate; VAS, Visual analog scale; yrs, Years. (Elements of table used in: Rabago D, Best T, Beamsley M, Patterson J. Systemic review of prolotherapy for chronic musculoskeletal pain. Clin J Sport Med, 15(5): 376-380; 2005.)

120  Complementary and Alternative Medical Procedures

Table 15-1  Description of Case Reports and Case Series—cont’d

Prolotherapy: A CAM Therapy for Chronic Musculoskeletal Pain  121

15

Table 15-2  Description of Controlled, Non-randomized Prolotherapy Studies Study

Indication

Subjects

Injectant

Outcome Measures

Results

Naeim et al., 1982120

SI dysfunction

3 M, 13 F; ages 19-80 yrs

Control: 9 subjects treated with lidocaine injections Intervention: 7 subjects treated with lidocaine and dextrose injections

2-item scale: “good” subjective improve­ ment, able to conduct daily activities, without pain, no pain medication needed, and negative clinical signs; “poor” results if the above not met

Lidocaine alone: good: 4/9 (44%), poor: 5/9 (56%); lidocaine and dextrose: good: 6/7 (86%), poor: 1/7 (14%)

Yelland et al., 200024

LBP

20 M, 13 F; ages 37-63 yrs; pain for 36-120 mos

Control: 13 subjects treated with conservative LBP modalities Intervention: 20 subjects treated with dextrose injec­ tions

VAS on pain intensity; Pain Diagram Disability Score; General Quality of Life score; percentage reaching 50% improvement in pain

Improvement in: VAS leg pain (P <.05), pain diagram (P = .05), LBP (P = .07) and disability scores (P = .08) com­ pared to controls

LBP, Low back pain; SI, Sacroiliac; VAS, Visual analog scale. (Elements of table used in: Rabago D, Best T, Beamsley M, Patterson J. Systemic review of prolotherapy for chronic musculoskeletal pain. Clin J Sport Med, 15(5): 376-380; 2005.)

24 21 18

Randomized controlled trials

15

Non-randomized controlled trials

12

Case reports

9 6 3 0 1930s 1940s 1950s 1960s 1970s 1980s 1990s 2000s Decade Figure 15-3  Number of published clinical studies on prolotherapy since 1937. (Bar graph from: Rabago D, Slattengren A, Zgierska A. Prolotherapy in primary care practice. Primary Care, 37(1); 69-80; 2010.)

Tendinopathies The strongest data supporting the efficacy of prolotherapy for any musculoskeletal condition, compared to control injections, is for chronic, painful overuse tendon conditions that were formerly called “tendonitis” and are now more correctly termed tendinosis or tendinopathy to reflect existing, underlying pathophysiology.27 Tendinopathies are common reasons why patients present to primary care providers and various medical specialists.28,29 Tendinopathies are sometimes discussed as a group because the current understanding of over-use tendinopathies identifies them as sharing underlying non-inflammatory pathology, resulting from a repetitive motion or overuse injury, and associated with painful degenerative tissue. Histopathology of tendon biopsies in patients undergoing surgery for painful tendinopathy reveals collagen separation,30 thin, frayed, and fragile tendon fibrils, separated from each other lengthwise and disrupted in cross-section, increase in tenocytes with myofibroblastic differentiation (tendon repair cells), proteoglycan ground substance, and neovascularization. Classic inflammatory cells are usually absent.30 Although this aspect of tendinosis was first described 25 years ago31 and content experts have advocated a change in nomenclature (from “tendonitis” to tendinosis),27 use of

the term “tendonitis” continues.32 Prolotherapy has been assessed as a treatment for four tendon disorders: lateral epicondylosis, hip adductor, Achilles tendinopathies, and plantar fasciitis (see Tables 15-1 and 15-3). Lateral epicondylosis (LE, “tennis elbow”) is an important common condition of the upper extremity with an incidence of 4 to 7 per 1000 patients per year in primary care settings.33-35 Its greatest impact is on workers with repetitive and high-load upper extremity tasks and on athletes. Its most common cause may be low-load, high-repetition activities such as keyboarding, although formal data are lacking.36 Cost and time away from job or activity are significant.37,38 While many nonsurgical therapies have been tested for LE refractory to conservative measures, none have proved uniformly effective in the long term.39-41 Scarpone and colleagues conducted an RCT to determine whether prolotherapy improves self-reported elbow pain, and objectively measured grip strength and extension strength in patients with chronic LE (see Table 15-3). Twenty adults with at least 6 months of moderate-to-severe painful LE refractory to rest, NSAIDs, and corticosteroid injections, were randomized to prolotherapy with dextrose and morrhuate sodium (1 part 5% sodium morrhuate, 1.5 parts 50% dextrose, 0.5 parts 4% lidocaine, 0.5 parts 0.5% bupivacaine, and 3.5 parts normal saline) or control injections with normal saline. Three prolotherapy sessions were administered, with injection at the supracondylar ridge, lateral epicondyle, and annular ligament. Compared to controls, prolotherapy subjects reported significantly decreased pain scores at 8 and  16 weeks. These between-group differences in pain scores were associated with a significant improvement in prolotherapy subjects (from 5.1 ± 0.8 points at baseline, down to 0.5 ± 0.4 points at  16 weeks), whereas the controls did not report significant change (4.5 ± 1.7 points to 3.5 ± 1.5 points). In addition to pain reduction, prolotherapy subjects also showed significantly improved isometric strength compared to controls and improved grip strength compared to baseline. These clinical improvements seen in prolotherapy subjects were maintained at 52 weeks. Two other recent evaluations of prolotherapy for LE have been performed. In a small RCT, Glick and coworkers reported 66% improvement on a disease specific questionnaire compared to 11.5% for controls (P =.09) receiving sham injections (see Table 15-3). This unpublished study formed the pilot data for a National Institutes of Health study now under way. (Prolotherapy for the treatment of chronic lateral epicondylitis; 1R21AT003969-01A1). In a

Table 15-3    Randomized Controlled Trials Assessing Prolotherapy for Tendinopathy, Low Back Pain, and Osteoarthritis Study/ Type

Subjects

Intervention

Injectant/Control

Ancillary Treatment

Scarpone et al. 200810

24 (13 F); mean age 45.7 (19-62) yrs; LE pain for mean 1.9 yrs; failed NSAIDs, relative rest, PT,   2 steroid injec­ tions

PrT: at 0, 4, 8 wks, to tender points at supracondylar ridge, lateral epicondyle and annular ligament; 1.5 mL total

PrT: 10.7% dextrose + 14.7% sodium mor­ rhuate Control: 0.9% saline

None

Glick et al., 2006121

8 (2 F), mean age 50; LE pain for greater than 3 mos

PrT: at 0, 3 and 6 wks to the lateral epicondyle and tender extensor tendon origin; 5 mL total

PrT: 15% dextrose and 1% lidocaine Control: 0.9% saline and 1% lidocaine

Yelland   et al., 201013

43 adult subjects age 40-58 (mean 46) yrs; midsubstance Achilles pain for 14.3-51 (mean 21) mos with moderateto-severe pain

Subjects random­ ized to eccentric exercise or cuta­ neous prolother­ apy or combined therapy

Ongley et al., 198752

38 M, 43 F with LBP; average age 44 yrs; pain for (average) 10 yrs

6 weekly injection series; up to 20 mL per series to lumbosacral liga­ ments

Followup/­Outcome ­Measures

Delphi score, x/9

Results

Limitations

8, 16, 52 wks resting elbow pain (0-10 VAS); isometric strength; grip strength; continuity of improvement at 52 wks

At 16 wks, pain improved   (P < .05) by 4.6 points c/t baseline, and 3.6 points c/t control; at 16 wks, isometric strength improved (P < .05) c/t base­ line and control; grip strength improved (P < .05) c/t baseline; at 52 wks, qualitative improvement c/t control

Lack of consistent, long-term follow-up; unconventional assessment of grip strength

8

All subjects used at-home stretching

9 wks; McGill Pain Questionnaire (0-45), Physical Composite score of MOS SF-36

McGill score improved (P = .086) by 7.75 points c/t baseline and 7 points c/t control Physical Composite score improved (P = .05) by 8.4 points c/t baseline and control. Cohen’s d statistic calculated to be 1.57 and 1.78 for the McGill and MOS measures respectively

Lack of diseasespecific outcome measure, short follow-up period

7

Prolotherapy: 20% dextrose/0.1% lido­ caine/0.1% ropivacaine; 0.5-1.0 mL injected along tender points to a total of 5 mL No placebo control

None

Victorian Institute of Sport AssessmentAchilles (VISA-A) validated questionnaire; economic analysis

VISA-A: mean (95% CI) improvement in overall severity scores at 12 mos were 23.7 (15.6 to 31.9) for eccentric exercise, 27.5 (12.8 to 42.2) for prolotherapy, and 41.1 (29.3 to 52.9) for combined treatment   (P < .01) Combined treatment had the lowest incremental cost per additional responder compared with eccentric exercise alone

P2G Saline/lidocaine

Intervention group: initially 60 mL lidocaine injection and force­ ful spinal manipulation, followed by triamcinolone/lidocaine injection. Control group: initially 10 mL lidocaine injection, followed by nonforceful spinal manipulation; both groups encouraged to do routine activity and 150 flexion exercises daily

1, 3, 6 mos

Percentage of subjects achieving 50% pain reduction; VAS pain intensity; Roland-Morris Disability Scale; clinical signs (ROM, tenderness).

9

Lack of noninjection control group; different ancillary interventions for intervention and control groups making these groups noncomparable

7

Klein,   et al., 199353

47 M, 32F with LBP; average age 44 yrs; pain for (average) 11 yrs

6 weekly injection series ; up to 30 mL per series to lumbosacral ligaments

P2G Saline/lidocaine

Initial spinal manipulation for all subjects, followed by steroid injection at tender points; all subjects advised to do back exercises

6 mos

Percentage of subjects achieving 50% pain reduction; VAS pain intensity; Roland-Morris Disability Scale; pain grid; ROMh by triaxial dynamometer

Lack of noninjection control group; experimental group had statistically worse baseline pain

7

Dechow , et al., 199954

36 M, 38 F with LBP; average age 46 yrs; pain for (average) > 10 yrs

Up to 3 weekly injection series; up to 10 mL per series to lumbosacral ligaments

P2Gf Saline/lidocaine

None

1, 3, 6 mos

Percentage of subjects achieving 50% pain reduction; McGill Pain Questionnaire; pain drawing grid; Somatic Perception Questionnaire; Depression Scale; Owestry Disability Scale; objective assessment of ROM

Lack of nonin­ jection control group; data presented graphically, no numerical data for any outcomes; unclear blinding of allocation and prolotherapist

8

Yelland et al., 200455

63 M, 47 F with LBP; average age 50 yrs; pain for (average) 14 yrs

On average, 7 biweekly injection series to lumbosacral ligaments; 10-30 mL per series

20% dextrose and 0.2% lidocaine Saline

Subjects stratified in 2 × 2 factorial design to receive dextrose or saline injections with either flexion/extension exercises or normal activity; to receive specific back exercises vs. recommendations to stay generally “active” All subjects received daily oral vitamin C, zinc, and manganese supplements

2.5, 4, 6, 12, 24 mos

Percentage of subjects achieving 50% pain or disability reduction; prior week pain VAS; medication use; pain diagram; physical and mental health quality of life scale

Lack of noninjection control group

9

Reeves et al., 200020

39 M, 29 F with knee OA pain; average age 63 yrs; pain for minimum of 6 mos

Single 9 mL   Intra-articular injection to affected knee at 0, 2, and 4 mos

10% dextrose and 0.075% lidocaine in bacteriostatic H2O H2O/lidocaine

Injections at 6, 8, and 10 mos; unblinded follow-up

6, 12 mos

Multiple VAS assessments for knee pain, swelling, stability; leg buckling frequency; knee laxity arthrometry; joint space x-ray

Lack of noninjection control group; difficult to interpret the results of comparison between the groups

7

Reeves, et al., 200066

11 M, 16 F with finger OA pain; average age 64 yrs; pain for (average) 4-5 yrs

Average 6 periar­ ticular injections to DIP, PIP and/or CMC joints at 0, 2, and 4 mos

10% dextrose and 0.075% lidocaine in bacteriostatic H2O H2O/lidocaine

Injections at 6, 8, 10 and 12 mos, and as needed; unblinded follow-up

6, 12 mos

Pain scores at rest, with movement, grip and flexion; average pain score; ROM goniometry; joint space x-ray

Lack of noninjection control group

9

CMC, Carpometacarpal joint; DIP, Distal interphalangeal joint; LE, Lateral epicondylosis; NSAIDs, Nonsteroidal antiinflammatory drug(s); PIP, Posterior interphalangeal joint; PrT, please supply; ROM, Range of motion; VAS, Visual analog scale. (Elements of table used in: Rabago D, Best T, Beamsley M, Patterson J. Systemic review of prolotherapy for chronic musculoskeletal pain. Clin J Sport Med, 15(5): 376-380; 2005.)

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124  Complementary and Alternative Medical Procedures

Table 15-4  Strength of Evidence for Prolotherapy as a Treatment for Chronic Musculoskeletal Conditions: Low Back Pain (LBP), Osteoarthritis (OA), and Tendinopathy Key Clinical Recommendation on Prolotherapy

Evidence Rating

Reference(s)

Nonspecific LBP: may be effective; conflicting results in several RCTs

B

52, 53, 54, 55

Sacroiliac joint dysfunction: may be effective in patients with documented failure of load transfer (disability) at the sacroiliac joint

B

62

Coccygodynia: may be effective based on prospective case series

B

63

Lateral epicondylosis: likely effective based on strong positive data in these small RCTs

A

10

Achilles tendinopathy: may be effective based on high quality prospective case series

B

7,13

Plantar fasciitis: may be effective, based on high-quality prospective case series

B

12

Osteoarthritis: may be effective for knee and finger OA, based RCTs of moderately strong methodologic quality

B

20, 66

RCTs, Randomized controlled trials.

prospective case series, Lyftogt42 reported 94% improvement compared to baseline scores using a novel subcutaneous injection technique (P < .05) (see Table 15-1). Achilles tendinopathy is a common overuse injury seen in athletes and in the general population. This painful condition is a cause of considerable distress and disability.43 The strongest data supporting the use of prolotherapy for Achilles tendinopathy suggest that a combination of prolotherapy and eccentric exercise may be optimal treatment for this challenging condition. Yelland and colleagues13 compared the clinical and cost-effectiveness of eccentric loading exercises with prolotherapy injections (see Table 15-3). Forty subjects with painful mid-portion Achilles tendinosis completed a 12-week program of eccentric exercise (n = 15), or prolotherapy injections of hypertonic dextrose with lidocaine (n = 14) or combined treatment (n = 14). On a validated multidimensional survey, mean (95% CI) improvement in overall severity scores at 12 months were 23.7 (15.6 to 31.9) for eccentric exercise, 27.5 (12.8 to 42.2) for prolotherapy and 41.1 (29.3 to 52.9) for combined treatment. At 6 weeks and 12 months, these increases were significantly less for eccentric exercise than for combined treatment. Combined treatment also had the lowest incremental cost per additional responder compared with eccentric exercise alone. Maxwell and coworkers conducted a well-designed case series to assess whether prolotherapy, administered during a mean of four injection sessions at 6-week intervals would decrease pain in 36 adults with painful Achilles tendinopathy (see Table 15-1). In this study, 25% dextrose solution was injected into hypoechoic regions of the Achilles tendon under ultrasound guidance. In addition to self-reported measures, the authors also assessed ultrasound-based tendon thickness, and the degree of hypoechogenicity and neovascularity—ultrasound findings recently reported to correlate to tendinopathy severity.44,45 At 52 weeks, prolotherapy-treated subjects

reported decrease in VAS-assessed pain severity by 88%, 84%, and 78% during rest, “usual” activity, and sport, respectively. In addition, tendon thickness decreased significantly. The overall grade of tendon pathology, hypoechoic and anechoic tendon regions, and neovascularity were all improved in some, but not all, subjects who reported clinical improvement. Therefore, the relationship between ultrasound-assessed characteristics and the degree of clinical improvement remains unclear. Hip adductor tendinopathy, associated with groin pain, is a common problem among those who engage in kicking sports.46 Topol and associates conducted a case series assessing prolotherapy for chronic groin pain, a condition involving pain and tenderness at tendon and ligament insertions at the groin area (see Table 15-1).47 Male athletes (N = 24), with an average duration of 15.5 months of groin pain in spite of standard therapy, were injected with 12.5% dextrose at the thigh and suprapubic abdominal insertions of the adductor tendon and at the symphysis pubis at 4-week intervals until pain resolved or subjects had no improvement for two consecutive sessions. On average, subjects received three prolotherapy sessions. At a mean of 17 months, subjects reported dramatic significant improvements on two pain scales (VAS and the Nirschl Pain Phase Scale). Of 24 subjects, 20 had no pain and 22 returned to sports without restrictions after therapy. Plantar fasciitis is a common injury among athletes engaged in sports requiring running and among general primary care patients. It is reported to account for 15% of all adult foot complaints requiring professional consultation, and, in a 2002 survey of runningrelated injuries, plantar fasciitis was the third most prevalent injury.48,49 Among “standard of care” approaches, there is limited evidence for the effectiveness of any one treatment for plantar fasciitis, including steroid injections.50 Ryan and coworkers assessed prolotherapy for chronic plantar fasciitis refractory to conservative care.12 Twenty adults with an average of 21 months duration of heel pain underwent ultrasound-guided 25% dextrose injections for an average of three treatment sessions delivered at 6-week intervals (see Table 15-1). Pain scores were assessed, using a 100-point VAS, at baseline and at 11.8 months. Pain severity significantly improved at rest, during activities of daily living, and sport activities by 26.5, 49.7, and 56.5 points, respectively, compared to baseline, and 16 of 20 subjects reported good or excellent treatment effects. Low Back Pain Low back pain (LBP) is among the most common reasons patients see a primary care provider. Approximately 80% of Americans experience LBP during their lifetime. An estimated 15% to 20% of patients develop protracted pain, and approximately 2% to 8% experience chronic pain. LBP is second only to the common cold as a cause of lost work time. Productivity losses from chronic LBP approach $28 billion annually in the United States.51 Low back pain was the first condition to be evaluated using prolotherapy in an RCT context. Early studies reporting positive results suffered from confusing methodology or unclear reporting styles; the strongest study reported trends favoring prolotherapy compared to control groups without significant differences. More recent prospective case series reporting positive results compared to baseline conditions have attempted to refine inclusion criteria to better determine which, if any, patients benefit from prolotherapy (Tables 15-1, 15-2, and 15-3). Nonspecific LBP. Four RCTs evaluated prolotherapy for musculoskeletal LBP; three used P2G as the injectant52-54 and the fourth used dextrose.55 Each study used a protocol involving injections to the ligamentous insertions of the L4-S1 spinous processes, sacrum,

Prolotherapy: A CAM Therapy for Chronic Musculoskeletal Pain  125

and ilium. Although outcome measures varied, a common measure was the percentage of participants reporting greater than 50% improvement in pain/disability scores at 6 months. Two of these four RCTs reported positive findings compared to control injections. Ongley and coworkers52 and Klein and associates53 compared the treatment effects of prolotherapy combined with an adjacent treatment with injected steroids, spinal manipulation, and exercise. In the Ongley study,52 the intervention and control groups differed markedly on the make-up of initial injections and type of spinal manipulation associated with the injections. Significantly more subjects in the prolotherapy (88%) group reported at least 50% reduction in pain severity compared to controls (39%). Also, prolotherapy subjects, compared to controls, reported significantly decreased pain and disability levels.52 Klein and associates,53 used more similar treatment protocols in the two assessed groups, with subjects in both groups receiving steroid injections and spinal manipulation prior to prolotherapy. Again, significantly more prolotherapy subjects improved by 50% or more on pain or disability scores (77%) than did controls (53%). Pain grid scores were also significantly lower in the prolotherapy group, with individual pain  (P = .06) and disability (P = .07) scores trending toward significance, compared to the control group. Two of the four RCTs reported negative outcomes compared to control injections.54,55 Dechow and colleagues54 implemented a refined study protocol; subjects in both groups underwent three injection therapy sessions without adjacent spinal manipulation or physical therapy. Although both groups showed a trend toward improved severity scores on pain questionnaire, pain grid, and somatic perception measures, these changes did not reach statistical significance over time within or between groups. At 6 months, improvements in both groups were less than those of the other RCTs. The largest and most methodologically rigorous prolotherapy study published to date has been conducted by Yelland and colleagues.55 Study subjects (N = 110), with an average of 14 years of LBP, were randomized to one of four intervention groups: dextrose and physical therapy, dextrose and “normal activity”, saline injections (“control” injection) and physical therapy, or saline injections and “normal activity”. By 12 months, subjects in all groups reported improvement in pain level (26% to 44%) and disability (30% to 44%) scores, without significant differences between groups. The majority of subjects (55%) stated that their improvement in regard to pain and disability had been worth the effort of undergoing the intervention. The percentage of subjects who reached at least 50% pain reduction varied between 36% and 46%, although these differences were not statistically significant. Overall, interpretation of findings from these four RCTs is challenging. Both experimental and control groups received different treatment protocols, and none of the trials was designed to elicit a possible mechanism of prolotherapy action. Therefore, it is impossible to attribute effects to prolotherapy or any other specific intervention. A recent Cochrane Collaboration systematic review56 did not find sufficient evidence to recommend prolotherapy for nonspecific LBP. However, these four RCTs present overall promising results, calling for well-designed, sufficiently-powered research. All RCTs report improvements for pain and disability in all treatment groups consisting of subjects with chronic, moderate-to-severe LBP. In particular, Yelland and colleagues55 reported clinical improvement in excess of minimal clinical important difference,57-59 and in excess of subjects’ own perception of the minimum improvement necessary for prolotherapy to be worthwhile (25% for pain and 35% for disability).24,55

Specific Causes of Low Back Pain Prolotherapy research methods for LBP have progressed amid much debate surrounding effectiveness, indications, treatment protocols, and solution types.60,61 Given the promising aspects of the above RCTs for nonspecific LBP, combined with anecdotal clinical success, recent clinical researchers have begun to assess prolotherapy in patients with more specific forms of LBP and loss of function in an effort to determine which specific causes of LBP are most responsive to prolotherapy. Cusi and colleagues assessed 25 subjects with sacroiliac joint dysfunction and pain, refractory to 6 months or more of physical therapy, and with documented failure of load transfer (disability) at the sacroiliac joint.62 They used a relatively strong prolotherapy solution of 18% dextrose, delivered in three sets of injections over 12 weeks. Compared to baseline, pain and disability scores on three multidimensional outcome measures significantly improved at 26  month follow-up in excess of minimal clinically important difference. Khan and colleagues assessed 37 subjects with refractory coccygodynia.63 Using 25% dextrose in up to three prolotherapy injection sessions over 2 months, average pain scores (evaluated using a 0 to 10 visual analog scale [VAS]), significantly decreased from a baseline score of 8.5 to 2.5 points at 2 months, far in excess of reported minimal clinical important difference for chronic pain.64 The authors reported “good” pain relief for 30 of 37 subjects, and “no improvement” for those remaining.7 In an especially novel study, Miller and colleagues assessed prolotherapy for leg pain due to moderate-to-severe degenerative disc disease as determined by computed tomography.65 Subjects (N = 76) who failed physical therapy and had substantial but temporary pain relief with two fluoroscopically-guided epidural steroid injections were included. After an average of 3.5 sessions of biweekly, fluoroscopically-guided injections to the relevant disc space with 25% dextrose with bupivacaine, 43% of responders showed a significant, sustained treatment response of 71% improvement in pain score, with VAS score for responders at 8.9 (±1.4), 2.5  (±2.0), and 2.6 (±2.2) at baseline, 2 and 18 months, respectively. Although these three recent studies of prolotherapy for “specific” LBP were uncontrolled, they suggest the need for future RCTs with more focused clinical indications of axial pain and disability. Osteoarthritis Prolotherapy has been assessed as a treatment for knee and finger osteoarthritis20,66 and is the subject of ongoing studies.67 Arthritis is a leading cause of disability in the world and in the United States where it affects 43 million people.68-70 Osteoarthritis (OA) is the most common form of arthritis and the most common joint disorder.71 In the United States, symptomatic knee OA is present in up to 6% of the population older than 30 years,71 and has an overall incidence of 360,000 cases per year.72 Incidence increases up to 10-fold from ages 30 to 65 and more thereafter.73 OA results in a high burden of disease and substantial economic impact through its high prevalence, time lost off work, and frequent use of health care resources.68,74 Allopathic and CAM treatment recommendations for OA, aimed at correcting modifiable risk factors, symptom control, and disease modification, have been published.75,76 Although these modalities may help some patients, none provides definitive pain control or disease modification for patients with knee OA. The Agency for Healthcare Research and Quality (AHRQ) has recently evaluated the most common standard treatment options including glucosamine, chondroitin, viscosupplementation, and arthroscopic débridement.77 These have not proven to be superior to placebo. The high burden of

15

126  Complementary and Alternative Medical Procedures

knee OA and the absence of cure continue to stimulate intense search for new agents to modify disease and control symptoms. Reeves and colleagues assessed prolotherapy as a treatment for knee and finger OA.20,66 Subjects with finger or knee pain and radiologic evidence of OA were randomly assigned to receive three injection sessions of either prolotherapy with 10% dextrose and lidocaine, or lidocaine and bacteriostatic water (control group). In the knee OA trial, subjects in both groups reported significant improvements in pain and swelling scores, number of buckling episodes, and flexion range of motion compared to baseline, but without statistically significant differences between the groups. Surprising and potentially important 12-month follow-up in both studies included improved radiologic features of OA on plain x-ray films: authors reported decreased joint space narrowing and osteophyte grade in the finger study, and increased patellofemoral cartilage thickness in the knee study. These radiologic findings suggest disease modification properties of prolotherapy. However, whether or not subjects in the knee study had a baseline concomitant meniscal pathology was not reported or included in entry criteria. Furthermore, the ability of plain radiographs to quantify patellofemoral cartilage thickness is questionable, thereby limiting the impact of these findings. In the finger OA trial, intervention subjects significantly improved in “pain with movement” and “flexion range” scores compared to controls; pain scores at rest and with grip showed a tendency to improvement without reaching statistical significance. A more rigorous set of knee OA assessments is currently under way. Rabago and colleagues are conducting an NIH-NCCAM sponsored RCT assessing prolotherapy for knee OA using a more complex “whole organ” clinical and assessment approach (“The efficacy of prolotherapy for osteoarthritic knee pain;” NIH-NCCAM 5K23AT001879-05). Although degeneration of articular cartilage is a hallmark of knee OA, the pathology of other structures in and around the knee joint may also contribute to the pain and disability of knee OA, including osteophytes, subchondral cysts, joint effusions, ligament and tendon tears, Baker cysts, synovitis, meniscal tears, and subchondral bone marrow edema within the knee joint.78-83 Therefore, the injection protocol includes a comprehensive set of extra- and intra-articular injections (Figs. 15-1 and 15-2). The results of prolotherapy injections will be compared to those of subjects in two other groups receiving control saline injections and at-home physical therapy injections, respectively. The primary outcome will be the Western Ontario and McMaster University Osteoarthritis Index (WOMAC)84 questionnaire. Magnetic resonance imaging has been identified as an appropriate imaging modality with which to evaluate disease-modifying OA therapies in clinical trials.79,85,86 This study will assess the changes in response to prolotherapy using validated clinical assessment and magnetic resonance imaging in a subset of subjects.

common clinically but its incidence has not been well documented. An ongoing study of prolotherapy for knee OA pain has noted that 10% to 20% of subjects experience such flares.122 Pain flares are likewise typically self-limited and usually respond well to acetaminophen (500 to 650 mg every 4 hours as needed). On rare occasions, the occurrence of strong, post-injection pain may require treatment with narcotic medication. Nonsteroidal antiinflammatory agents are not routinely used after the procedure but may be indicated if the pain does not resolve with other measures. Most patients with pain flares experience diminution of pain in 5 to 7 days after injections; regular activities can be progressively resumed at this time.

Adverse Events While prolotherapy performed by an experienced injector appears to be safe, the injection of ligaments, tendons, and joints with irritant solutions raises safety concerns. Theoretic risks of prolotherapy injections include lightheadedness, allergic reaction, infection, or neurological (nerve) damage. Injections should be performed using universal precautions and the patient should be prone if possible. Dextrose is extremely safe; it is approved by the Food and Drug Administration (FDA) for intravenous treatment of hypoglycemia and for caloric supplementation.123 As of 1998, FDA records for intravenous 25% dextrose solution reported no adverse events to Abbott Laboratories in 60 years.124 Morrhuate sodium is a vascular sclerosant used in gastrointestinal procedures and vein sclerosing. Allergic reactions to morrhuate sodium are rare. Although P2G is not FDA approved for any indication, it has not been reported in clinical trials to cause significant side effects or adverse events. Historically, a small number of significant, prolotherapy-related complications have been reported. They were associated with perispinal injections for back or neck pain, using highly concentrated solutions, and included five cases of neurologic impairment from spinal cord irritation125-127 and one death in 1959 following prolotherapy with zinc sulfate for low back pain.125 Neither zinc sulfate nor concentrated prolotherapy solutions are currently in general use. In a survey of 95 clinicians using prolotherapy, there were  29 reports of pneumothoraces after prolotherapy for back and neck pain, 2 of which required hospitalization for a chest tube, and  14 cases of allergic reactions, although none were classified as ­serious.5 A more recent survey of practicing prolotherapists yielded similar results for spinal prolotherapy: spinal headache, pneumothoraces, nerve damage and nonsevere spinal cord insult, and disc injury were reported.128 The authors concluded these events were no more common in prolotherapy than for other spinal injection procedures. No serious side effects or adverse events were reported for prolotherapy when used for peripheral joint indications.

Contraindications

Side Effects, Adverse Events, and Contraindications Common Side Effects The main risk of prolotherapy is pain and mild bleeding as a result of needle trauma. Patients frequently report pain, a sense of fullness, and occasional numbness at the injection site at the time of injections. These side effects are typically self-limited. A postinjection pain flare during the first 72 hours after the injections is

Absolute contraindications to prolotherapy are few and include acute infections such as cellulitis, local abscess or septic arthritis. Relative contraindications include acute gouty arthritis and acute fracture.

Prolotherapy in Practice Similar to corticosteroid injections, prolotherapy is an unregulated procedure without certification by any governing body. Formal training is not provided by most medical schools, residencies, and fellowships. However, prolotherapy, to be performed appropriately

Prolotherapy: A CAM Therapy for Chronic Musculoskeletal Pain  127

15

Table 15-5  Educational and Informational Prolotherapy Resources Name/URL

Comments

“The Anatomy, Diagnosis, and Treatment of Chronic Myofascial Pain with Prolotherapy” http://www.ocpd.wisc.edu/Course_Catalog/

Continuing medical education (CME) on the basics of prolotherapy. This 3.5 day conference is offered through the University of Wisconsin School of Medicine and Public Health. All aspects of clinical and research aspects of prolotherapy are covered.

Hackett Hemwall Foundation List of Prolotherapists http://www.hacketthemwall.org/HHF/List_of_Prolotherapists.html

The Hackett Hemwall Foundation is a nonprofit medical foundation whose mission is to provide high-quality treatment of musculoskeletal problems to underserved people around the world. Physicians listed on the site have completed the Foundation’s high-volume continuing medical education experience in prolotherapy.

Commercial Prolotherapy Physician Listing http://www.getprolo.com

This site lists physicians by state who perform prolotherapy. It includes contact information and a short biography and ­prolotherapy credentials. Physicians pay to list themselves on this site.

American Association of Orthopaedic Medicine http://www.aaomed.org

The American Association of Orthopaedic Medicine is a nonprofit organization that provides information and educational programs on comprehensive nonsurgical musculoskeletal treatment including prolotherapy. This searchable site lists AAOM members who perform prolotherapy.

and safely, requires specialized training. In the United States, it is taught to physicians and other health care providers (authorized to deliver joint-type injections) in semiformal workshops and formal continuing medical education (CME) by several organizations, including university settings (Table 15-5). Patients and physicians who desire consultation for prolotherapy may have difficulty finding an appropriate consulting prolotherapist. Online resources (see Table 15-5) are available that can help locate a prolotherapist, although information is limited by lack of a credentialing structure and governing body for prolotherapy. Despite limited institutional support, interest in prolotherapy is increasing, and it is performed in increasing numbers, primarily in two settings. For several decades, prolotherapy has been mostly performed outside of mainstream medicine by independent physicians. More recently, multispecialty groups that include family or sports medicine physicians, physiatrists, orthopedic surgeons, neurologists, or anesthesiologists have been incorporating prolotherapy as a result of positive clinical experience and research reports. Prolotherapy is one of several injection therapies that may promote healing of chronically injured soft tissue. Other therapies receiving active clinical and research attention for chronic musculoskeletal pain include whole blood, plateletrich plasma and polidocanol injections.11 In both settings, prolotherapy is viewed as a valued procedure, primarily reserved for patients who have failed other treatments or in patients who are not surgical candidates.

The Authors’ Clinic The authors practice in a community in which several primary care physicians and specialists perform prolotherapy; receptivity to prolotherapy in our setting is growing. Some health insurance plans in our area cover prolotherapy on a “prior authorization” basis for the indications discussed. Most payment is made “out-of-pocket”. Referrals can be made similarly to those for more conventional procedures. An initial consultation, including a focused history and physical examination, is performed by the prolotherapist to determine if the patient is a candidate for prolotherapy. If so, side effects, adverse events, and expected course of injections are explained, and the patient is asked to sign a procedure consent form. The patient is then scheduled for up to three outpatient prolotherapy

sessions, typically 4 to 6 weeks apart. At each subsequent visit, an interval history is obtained and physical examination is performed. If the patient does not report improvement after three prolotherapy sessions, alternative interventions are pursued.

Clinical Recommendations Present data suggest that prolotherapy is likely an effective therapy for painful overuse tendinopathy. Specifically, Scarpone and colleagues10 provide level A evidence for prolotherapy as an effective therapy for lateral epicondylosis. Subjects with refractory lateral epicondylosis and treated with prolotherapy reported significant reduction in pain and improved isometric strength compared to those who received control injections. These findings are supported by the Yelland,13 Maxwell,7 Topol,47 and Ryan12 studies that report strong case series results for Achilles, hip adductor, and plantar fasciitis, respectively, and provide level B evidence for these conditions. Given that the underlying mechanism of injury and pathophysiologic effects are likely similar for tendinopathies, prolotherapy is a reasonable option for other overuse tendinopathies as well. Randomized controlled trials for all three tendinopathies and for other tendinopathies are indicated. Recommendations are more difficult to make for osteoarthritis and low back pain, both of which are associated with more complex anatomy and less clear pathophysiology than that seen in tendinopathies. Side effect and potential adverse events of prolotherapy are likely to be more serious when performed for spinal or intra-articular indications and must be weighed against the potential for improvement. Existing studies provide level B evidence that prolotherapy is effective for nonspecific low back pain compared to a patient’s baseline condition. Given that subjects with refractory, disabling low back pain significantly improved compared to their own baseline status in the Yelland study,55 patients may reasonably try prolotherapy when performed by an experienced injector. Future studies with more focused inclusion criteria may help determine which specific low back pathologies respond to prolotherapy. Existing studies provide level B evidence that prolotherapy is effective for knee and finger osteoarthritis compared to control injections.20,66 Prolotherapy by an experienced physician is a treatment modality worthy of consideration by primary care physicians for these conditions, especially when patients are refractory to more conventional therapy.

128  Complementary and Alternative Medical Procedures

ACKNOWLEDGMENTS We acknowledge the support of Jessica Grettie, BS, for her ongoing efforts in prolotherapy research.

REFERENCES 1. Hackett GS, Hemwall GA, Montgomery GA. Ligament and tendon relaxation treated by prolotherapy. 5th ed. Oak Park, Ill: Hemwall; 1993, Gustav A. 2. Linetsky FS, Frafael M, Saberski L. Pain management with regenerative injection therapy (RIT). In: Weiner RS, ed. Pain Management. Boca Raton, Fla: CRC Press; 2002:381-402. 3. Matthews JH. Nonsurgical treatment of pain in lumbar spinal stenosis. Am Fam Physician. 1999;59(2):280-284. 4. Schnirring L. Are your patients asking about prolotherapy? Physician Sportsmed. 2000;28(8):15-17. 5. Dorman TA. Prolotherapy: A survey. J Orthop Med. 1993;15(2):49-50. 6. Linetsky FS, Botwin K, Gorfine L, Jay GW, et al. Regenerative injection therapy (RIT): Effectiveness and appropriate usage. Florida Acad Pain Med. 2001, http://fapmmed.net/Position.htm. 7. Maxwell NJ, Ryan MB, Taunton JE, et al. Sonographically guided intratendinous injection of hyperosmolar dextrose to treat chronic tendinosis of the Achilles tendon: A pilot study. AJR Am J Roentgenol. 2007;189(4):W215-220. 8. Jensen KT, Rabago DP, Best TM, et al. Early inflammatory response of knee ligaments to prolotherapy in a rat model. J Orthop Res. 2008;26: 816-823. 9. Jensen KT, Rabago DP, Best TM, et al. Response of knee ligaments to ­prolotherapy in a rat injury model. Am J Sports Med. 2008;36: 1347-1357. 10. Scarpone M, Rabago D, Zgierska A, et al. The efficacy of prolo­therapy for lateral epicondylosis: A pilot study. Clin J Sport Med. 2008;18: 248-254.   11. Rabago D, Best TM, Zgierska A, et al. A systematic review of four injection therapies for lateral epicondylosis: Prolotherapy, polidocanol, whole blood and platelet rich plasma. Br J Sports Med. 2009;43: 471-481.   12. Ryan MB, Wong AD, Gillies JH, et al. Sonographically guided intratendinous injections of hyperosmolar dextrose/lidocaine: A pilot study for the treatment of chronic plantar fasciitis. Br J Sports Med. 2009;43:303-306.   13. Yelland MJ, Sweeting KR, Lyftogt JA, et al. Prolotherapy injections and eccentric loading exercises for painful Achilles tendinosis: A randomised trial. Br J Sports Med. 2010 Jul 6 [Epub ahead of print].   14. Liu YK, Tipton CM, Matthes RD, et al. An in-situ study of the influence of a sclerosing solution in rabbit medial collateral ligaments and its junction strength. Connect Tissue Res. 1983;11:95-102.   15. Maynard JA, Pedrini VA, Pedrini-Mille A, et al. Morphological and biochemical effects of sodium morrhuate on tendons. J Orthop Res. 1985;3:236-248.   16. Banks A. A rationale for prolotherapy. J Orthop Med. 1991;13(3):54-59.   17. Hoksrud A, Ohberg L, Alfredson H, Bahr R. Ultrasound-guided sclerosis of neovessels in painful chronic patellar tendinopathy: a randomized controlled trial. Am J Sports Med. 2006;34:1738-1746.   18. Zeisig E, Fahlström M, Ohberg L, Alfredson H. A 2-year sonographic follow-up after intratendinous injection therapy in patients with tennis elbow. Br J Sports Med. 2010;44:584-587.   19. Kim SR, Stitik TP, Foye PM, et al. Critical review of prolotherapy for osteoarthritis, low back pain, and other musculoskeletal conditions:  A ­physiatric perspective. Am J Phys Med Rehabil. 2004;83(5):379-389.   20. Reeves KD, Hassanein K. Randomized prospective doubleblind placebo-controlled study of dextrose prolotherapy for knee osteoarthritis with or without ACL laxity. Altern Ther Health Med. 2000;6(2):68-80.   21. Aneja A, Karas SG, Weinhold PS, et al. Suture plication, thermal shrinkage and sclerosing agents: effects on rat patellar tendon length and biomechanical strength. Am J Sports Med. 2005;33:1729-1734.

  22. Jensen KT. PhD Dissertation: Healing response of knee ligaments to prolotherapy in a rat model. Madison, Wisc: Biomedical Engineering, University of Wisconsin; 2006.   23. Rabago D, Best TM, Beamsley M, Patterson J. A systematic review of prolotherapy for chronic musculoskeletal pain. Clin J Sports Med. 2005;15(5):376-380.   24. Yelland M, Yeo M, Schluter P. Prolotherapy injections for chronic low back pain: Results of a pilot comparative study. Aust Musculoskel Med. 2000;5(2):20-23.   25. Ernst E, Pittler MH, Stevinson C, White A. Randomised clinical trials: Pragmatic or fastidious? Focus Altern Complementary Ther. 2001;6:179-180.   26. Verhagen AP, de Vet HC, de Bie RA, et al. The Delphi list: A criteria list for quality assessment of randomized trials conducting reviews developed Delphi consensus. J Clin Epidemiol. 1998;51(12):1235-1241.   27. Khan KM, Cook JL, Kannus P, et al. Time to abandon the ‘tendinitis’ myth. BMJ. 2002;324:626-627.   28. Bongers PM. The cost of shoulder pain at work. Variation in work tasks and good job opportunities are essential for prevention. BMJ. 2001;322:64-65.   29. Wilson JJ, Best TM. Common overuse tendon problems: A review and recommendations for treatment. Am Fam Physician. 2005;72:811-818.   30. Khan KM, Cook JL, Bonar F, et al. Histopathology of common tendinopathies. Update and implications for clinical management. Sports Med. 1999;27:393-408.   31. Puddu G, Ippolito E, Postacchini F. A classification of Achilles tendon disease. Am J Sports Med. 1976;4:145-150.   32. Johnson GW, Cadwallader K, Scheffel SB, Epperly TD. Treatment of lateral epicondylitis. Am Fam Physician. 2007;76:843-848.   33. Verhaar JA. Tennis elbow: Anatomical, epidemiological and therapeutic aspects. Int Orthop. 1994;18:263-267.   34. Hamilton PG. The prevalence of humeral epicondylitis: A survey in general practice. J R Coll Gen Pract. 1986;36:464-465.   35. Kivi P. The etiology and conservative treatment of humeral epicondylitis. Scand J Rehabil Med. 1983;15:37-41.   36. Gabel GT. Acute and chronic tendinopathies at the elbow. Curr Opin Rheumatol. 1999;11:138-143.   37. Ono Y, Nakamura R, Shimaoka M, et al. Epicondylitis among cooks in nursery schools. Occup Environ Med. 1998;55:172-179.   38. Ritz BR. Humeral epicondylitis among gas and waterworks employees. Scand J Work Environ Health. 1995;21:478-486.   39. Buchbinder R, Green S, White M, et al. Shock wave therapy for lateral elbow pain. Cochrane Database Syst Rev. 2002;(1):CD003524.   40. Smidt N, van der Windt DA, Assendelft WJ, et al. Corticosteroid injections, physiotherapy, or a wait-and-see policy for lateral epicondylitis: A randomised controlled trial. Lancet. 2002;359:657-662.   41. Struijs PA, Smidt N, Arola H, et al. Orthotic devices for the treatment of tennis elbow. Cochrane Database Syst Rev. 2002;(1):CD001821.   42. Lyftogt J. Subcutaneous prolotherapy treatment of refractory knee, shoulder and lateral elbow pain. Aust Musculoskel Med. 2007;12:110-112.   43. Kvist M. Achilles tendon injuries in athletes. Sports Med. 1994; 18:173-201.   44. Zeisig E, Ohberg L, Alfredson H. Extensor origin vascularity related to pain in patients with tennis elbow. Knee Surg Sports Traumatol Arthrosc. 2006;14:659-663.   45. Alfredson H, Ohberg L. Sclerosing injections to areas of neovascularization reduce pain in chronic Achilles tendinopathy: A double-blind randomised trial. Knee Surg Sports Traumatol Arthrosc. 2005;13:338-344.   46. Holmich P, Uhrskou P, Ulnits L. Effectiveness of active physical training as treatment of long-standing adductor-related groin pain in athletes: A randomized trial. Lancet. 1999;353:439-443.   47. Topol GA, Reeves KD, Hassanein KM. Efficacy of dextrose prolotherapy in elite male kicking-sport athletes with chronic groin pain. Arch Phys Med Rehabil. 2005;86:697-702.   48. Buchbinder R. Clinical practice. Plantar fasciitis. N Engl J Med. 2004;350:2159-2166.

Prolotherapy: A CAM Therapy for Chronic Musculoskeletal Pain  129   49. Taunton JE, Ryan MB, Clement DB, et al. A retrospective case-control analysis of 2002 running injuries. Br J Sports Med. 2002;36:95-101.   50. Crawford F, Thomson C. Interventions for treating plantar heel pain. Cochrane Database Syst Rev. 2003;3:CD000416.   51. Wheeler AH: Low Back Pain and Sciatica. http://www.emedicine.com/ neuro/topic516.htm. 2010.   52. Ongley MJ, Klein RG, Dorman TA, et al. A new approach to the treatment of chronic low back pain. Lancet. 1987;2:143-146.   53. Klein RG, Eek BC, DeLong WB, Mooney V. A randomized doubleblind trial of dextrose-glycerine-phenol injections for chronic, low back pain. J Spinal Disord. 1993;6(1):23-33.   54. Dechow E, Davies RK, Carr AJ, Thompson PW. A randomized, double-blind, placebo-controlled trial of sclerosing injections in patients with chronic low back pain. Rheumatology. 1999;38:1255-1259.   55. Yelland MJ, Glasziou PP, Bogduk N, et al. Prolotherapy injections, saline injections, and exercises for chronic low back pain: A randomized trial. Spine. 2004;29(1):9-16.   56. Yelland MJ, Del Mar C, Pirozzo S, Schoene ML. Prolotherapy injections for chronic low back pain: A systematic review. Spine. 2004;29:2126-2133.   57. Bellamy N, Carr A, Dougados M, et al. Towards a definition of “difference” in osteoarthritis. J Rheumatology. 2001;28(2):427-430.   58. Redelmeier DA, Guyatt GH, Goldstein RS. Assessing the minimal important difference in symptoms: A comparison of two techniques.  J Clin Epidemiol. 1996;49:1215-1219.   59. Wells GA, Tugwell P, Kraag GR, et al. Minimum important difference between patients with rheumatoid arthritis: The patient’s perspective. J Rheumatol. 1993;20:557-560.   60. Loeser JD. Point of view. Spine. 2004;29(1):16.   61. Reeves KD, Klein RG, DeLong WB. Letter to the editor. Spine. 2004;29(16):1839-1840.   62. Cusi M, Saunders J, Hungerford B, et al. The use of prolotherapy in the sacroiliac joint. Br J Sports Med. 2010;44:100-104.   63. Khan SA, Kumar A, Varshney MK, et al. Dextrose prolotherapy for recalcitrant coccygodynia. J Orthop Surg. 2008;16:27-29.   64. Farrar JT, Young JP, LaMoreaux L, et al. Clinical importance of changes in chronic pain intensity measured on an 11-point numerical rating scale. Pain. 2001;94:149-158.   65. Miller MR, Mathews RS, Reeves KD. Treatment of painful advanced internal lumbar disc derangement with intradiscal injection of hypertonic dextrose. Pain Physician. 2006;9:115-121.   66. Reeves KD, Hassanein K. Randomized, prospective, placebo-controlled double-blind study of dextrose prolotherapy for osteoarthritic thumb and finger (DIP, PIP, and trapeziometacarpal) joints: Evidence of clinical efficacy. J Altern Complement Med. 2000;6(4):311-320.   67. Rabago D: The efficacy of prolotherapy in osteoarthritic knee pain. NIH-NCCAM Grant, 1K23 AT001879–01; 2004-2009; manuscripts in progress.   68. Reginster JY. The prevalence and burden of arthritis. Rheumatology. 2002;41(suppl 1):3-6.   69. Centers for Disease Control and Prevention (CDC): Prevalence and impact of chronic joint symptoms-seven states, 1996. MMWR Morb Mortal Wkly Rep. 1998;47:345-351.   70. Centers for Disease Control and Prevention (CDC). Prevalence of disabilities and associated health conditions—United States, 1991-1992. MMWR Morb Mortal Wkly Rep. 1994;43:730-739.   71. Felson DT, Zhang Y. An update on the epidemiology of knee and hip osteoarthritis with a view to prevention. Arthritis Rheum. 1998;41(8):1343-1355.   72. Wilson MG, Michet CJ, Ilstrup DM, Melton LJ. Ideopathic symptomatic osteoarthritis of the hip and knee: A population-based incidence study. Mayo Clic Proc. 1990;65:1214-1221.   73. Oliveria SA, Felson DT, Klein RA, et al. Estrogen replacement therapy and the development of osteoarthritis. Epidemiology. 1996;7: 415-419.   74. Levy E, Ferme A, Perocheau D, et al. Socioeconomic costs of osteoarthritis in France. [Article in French]. Rev Rhum Ed Fr. 1993;60:63S-67S.

  75. Felson DT, Lawrence RC, Hochberg MC, et al. Osteoarthritis: new insights, part 2: treatment approaches. Ann Intern Med. 2000;133:726-737.   76. Recommendations for the medical management of osteoarthritis of the hip and knee: 2000 update. American College of Rheumatology Subcommittee on Osteoarthritis Guidelines. Arthritis Rheum. 2000;43:1905-1915.   77. Samson DJ, Grant MD, Ratko TA, et al. Treatment of primary and secondary osteoarthritis of the knee. Evid Rep Technol Assess (Full Rep). 2007;157:1-157.   78. Hill CL, Gale DG, Chaisson CE, et al. Knee effusions, popliteal cysts, and synovial thickening: Association with knee pain in osteoarthritis.  J Rheumatol. 2001;28:1330-1337.   79. Guermazi A, Zaim S, Taouli B, et al. MR findings in knee osteoarthritis. Eur Radiol. 2003;13:1370-1386.   80. Hayes CW, Jamadar DA, Welch GW, et al. Osteoarthritis of the knee: Comparison of MR imaging findings with radiographic severity measurements and pain in middle-aged women. Radiology. 2005;237:998-1007.   81. Sowers MF, Hayes C, Jamadar D, et al. Magnetic resonance-detected subchondral bone marrow and cartilage defect characteristics associated with pain and x-ray-defined knee osteoarthritis. Osteoarthritis Cartilage. 2003;11:387-393.   82. Link TM, Steinbach LS, Ghosh S, et al. Osteoarthritis: MR imaging findings in different stages of disease and correlation with clinical findings. Radiology. 2003;226:373-381.   83. Wluka AE, Ding C, Jones G, Cicuttini FM. The clinical correlates of articular cartilage defects in symptomatic knee osteoarthritis: A prospective study. Rheumatology. 2005;44:1311-1316.   84. Bellamy N, Buchanan WW, Goldsmith CH, et al. Validation study of WOMAC: A health status instrument for measuring clinically important patient relevant outcomes in antirheumatic drug therapy in patients with osteoarthritis of the hip or knee. J Rheumatol. 1988;15:1833-1840.   85. Peterfy C, Woodworth T, Altman R. Workshop for consensus on osteoarthritis imaging: MRI of the knee. Osteoarthritis Cartilage. 2006;14:44-45.   86. Peterfy CG, Gold G, Eckstein F, et al. MRI protocols for whole-organ assessment of the knee in osteoarthritis. Osteoarthritis Cartilage. 2006(14):A95-A111.   87. Gedney E. Special technic hypermobile joint: a preliminary report. Osteopath Prof. 1937;4(9):30-31.   88. Shuman D. Luxation recurring in the shoulder. Osteopath Prof. 1941;8(6):11-14.   89. Bahme BB. Observations on the treatment of hypermotile joints by injection. J Am Osteopath Assoc. 1945;45(3):101-109.   90. Gedney EH. Disk syndrome: New approach in the treatment of symptomatic intervertebral disk. Osteopath Prof. 1951;18(12):11-14.   91. Gedney EH. Technique for sclerotherapy in the management of hypermobile sacroiliac. Osteopath Prof. 1952;19:37-38.   92. Hackett GS. Joint stabilization through induced ligament sclerosis. Ohio Med. 1953;49(10):877-884.   93. Shuman D. Sclerotherapy: Statisitics on its effectiveness of unstable joint conditions. Osteopath Prof. 1954;21:11-15:37–38.   94. Hackett GS. Shearing injury to the sacroiliac joint. J Int Coll Surg. 1954;22:631-642.   95. Neff F. Low back pain and disability. West Med. 1960;1:12-14:27-33.   96. Myers A. Prolotherapy treatment of low back pain and sciatica. Bull Hosp Joint Dis. 1961;22:48-55.   97. Hackett GS, Huang TC, Raftery A. Prolotherapy for headache. Pain in the head and neck, and neuritis. Headache. 1962;2:20-28.   98. Kayfetz DO, Blumenthal LS, Hackett GS, et al. Whiplash injury and other ligamentous headache—its managment with prolotherapy. Headache. 1963;3:21-28.   99. Kayfetz DO. Occipito-cerivical (whiplash) injuries treated by prolotherapy. Med Trial Tech Q. 1963;9:9-29. 100. Peterson TH. Injection treatment for back pain. Am J Orthop. 1963;5:320-321.

15

130  Complementary and Alternative Medical Procedures 101. Barbor R. A treatment for chronic low back pain. Paris: Paper presented at: Proceedings of IV Internationhal Congress of Physical Medicine; 1964;6-11. 102. Blumenthal L. Injury to the cervical spine as a cause of headache. Postgrad Med. 1974;56:147-153. 103. Leedy R, Kulik AL. Analysis of 50 low back cases 6 years after treatment by joint ligament sclerotherapy (prolotherapy). Osteopathic Med. 1976;6:15-22. 104. Leedy RF. Applications of sclerotherapy to specific problems. Osteopathic Med. 1977;2:79-97. 105. Leedy R. The challenge of a new skill. N Jersey Assoc Osteopat Phys Surg J. 1982;81(7):9-13. 106. Bourdeau Y. Five-year follow-up on sclerotherapy/prolotherapy for low back pain. Manual Med. 1988;3:155-157. 107. Ongley MJ, Dorman TA, Eck BC, et al. Ligament instability of knees: A new approach to treatment. Manual Med. 1988;3:152-154. 108. LaCourse M, Moore K, David K, et al. A report on the asymmetry of iliac inclincations. J Orthop Med. 1990;12(3):69-72. 109. Dorman TA. Treatment for spinal pain arising in ligaments-using prolotherapy: A retrospective study. J Orthop Med. 1991;13(1):13-19. 110. Schwartz RG, Sagedy N. Prolotherapy: A literature review and retrospective study. J Neurol Orth Med S. 1991;12:220-223. 111. Hirschberg GG, Williams KA, Byrd JB. Diagnosis and treatment of ileocostal friction syndromes. West J Med. 1992;14(2):35-39. 112. Reeves KD. Treatment of consecutive severe fibromyalgia patients with prolotherapy. J Orthopaedic Med. 1994;16(3):84-89. 113. Dorman TA, Cohen RE, Dasig D, et al. A. Energy efficiency during human walking before and after prolotherapy. J Orthop Med. 1995;17(1):24-26. 114. Matthews JN, Altman DG, Campbell MJ, Royston P. Analysis of serial measurements in medical research. BMJ. 1990;300:230-235. 115. Reeves KD, Harris AI. Recurrent dislocation of total knee prostheses in a large patient: Case report of dextrose proliferant use. Arch Phys Med Rehabil. 1997;78:1039. 116. Reeves KD, Hassanein KM. Long-term effects of dextrose prolotherapy for anterior cruciate ligament laxity. Altern Ther Health Med. 2003;9(3):58-62.

117. Hooper RA, Ding M. Retrospective case series on patients with chronic spinal pain treated with dextrose prolotherapy. J Altern Complement Med. 2004;10:670-674. 118. Hooper RA, Sherman ST, Frizzell JB. Case report of whiplash related chronic neck pain treated with intra-articular prolotherapy. J Whiplash Rel Disord. 2005;2:23-27. 119. Lazzara MA. The non-surgical repair of a complete Achilles tendon rupture by prolotherapy: biological reconstruction. A case report.  J Orthop Med. 2005;27:128-132. 120. Naeim F, Froetscher L, Hirschberg GG. Treatment of the chronic iliolumbar syndrome by infiltration of the iliolumbar ligament. West J Med. 1982;136(4):372-374. 121. Glick RM, Day RD, Stone DA, Cortazzo M. Prolotherapy for the treatment of lateral epicondylitis: A double-blind pilot study. Edmonton, Canada: Paper presented at: North American Research Conference on Complementary and Integrative Medicine; 2006. 122. Rabago D, Zgierska A, Mundt M, et al. Efficacy of prolotherapy for knee osteoarthritis: Results of a prospective case series (poster presentation). North American Research Conference on Complementary and Integrative Medicine. 2009. 123. AbbottLabs: FDA indications for 50% dextrose. http://www.fda.gov/ cder/foi/nda/98/19445-s4-s6.htm; 2004. 124. AbbottLabs: Approval documentation for 25% dextrose submitted to FDA by Abbott Laboratories. [Online documentation]. 125. Schneider RC, Williams JJ, Liss L. Fatality after injection of sclerosing agent to precipitate fibro-osseous proliferation. J Am Med Assoc. 1959;170(15):1768-1772:1959. 126. Keplinger JE, Bucy PC. Paraplegia from treatment with sclerosing agents—report of a case. JAMA. 1960;173(12):1333-1336. 127. Hunt WE, Baird WC. Complications following injection of sclerosing agent to precipitate fibro-osseous proliferation. J Neurosurg. 1961;18:461-465. 128. Dagenais S, Ogunseitan O, Haldeman S, et al. Side effects and adverse events related to intraligamentous injection of sclerosing solutions (prolotherapy) for back and neck pain: A survey of practitioners. Arch Phys Med Rehabil. 2006;87:909-913.

Percutaneous ­Neuromodulation Therapy

16

William M. Boggs, MD, and William F. Craig, MD

After using his own version of acupuncture for several years to treat complaints ranging from migraine headache to alcohol withdrawal to cancer pain, Craig decided in the late 1970s that he would develop a new system based on his belief that the effectiveness of electroacupuncture depended on its influence on the central nervous system. The new system was to be based on placing needles into the vicinity of nerves that conducted impulses away from the affected areas. The earliest recorded workshops called his technique “dermatomal electroacupuncture”. The system evolved through the years as Craig manipulated the key components of treatment, fine-tuning such important aspects as needle location, overall montage of needles employed, and stimulus frequency and duration. In parallel, other scientists advanced our understanding of the neurophysiology of chronic pain, elucidating the role of various neurotransmitters and the impact of electrical stimulation on the behavior of various nerve pathways. By the mid-1990s, dermatomal electroacupuncture had become percutaneous electrical nerve stimulation (PENS), which soon became Craig-PENS to honor Craig’s contribution. Besides indicating what the technique involved (percutaneous stimulation of nerves with electrical impulses), PENS emphasized the demarcation of this technique from acupuncture. Many practitioners continue to use PENS or Craig-PENS to describe what they do. A new millennium demanded a new acronym. At the turn of the century, Craig and colleagues renamed the technique Percutaneous Neuromodulation Therapy (PNT). This new moniker moved beyond description to explanation. PENS defines the technical performance of the method, but PNT explicates the neurophysiology behind why it works. Moreover, a new term was needed to distinguish an effective chronic pain treatment from a neurosurgical procedure involving implantable stimulating electrodes. This chapter will discuss PNT as developed by Craig and his associates. A word about acupuncture: although Craig studied acupuncture and initially called his technique dermatomal electroacupuncture, PNT should be distinguished from electroacupuncture. Unlike electroacupuncture, PNT does not involve needling of specific, traditional acupuncture points. In fact, as will be described later, placement of needles in PNT intends to influence dermatomal (or myotomal or sclerotomal) nerve pathways rather than acupuncture meridians. And PNT does not rely on the concept of "qi" or require any sort of traditional Chinese medicine (TCM) diagnosis. However, like electroacupuncture, PNT does involve needle insertion and electrostimulation, so the results of neurophysiologic studies of electroacupuncture also reflect the neuromodulatory impact of PNT. The importance of differentiating PNT from

electroacupuncture lies here: one need not undertake the study of acupuncture to to understand and practice PNT effectively.

How PNT Works As its name suggests, PNT is believed to work by modulation of central pain pathways using peripheral nerve stimulation. A body of neurophysiology research supports this presumption, and ongoing work continues to reveal details of the complex interactions that underlie the perception of pain. Peripheral nerve endings known as nociceptors sense pain and transmit signals to the dorsal root ganglion of the spinal cord. Localized, sharp, stinging pain, generally of short duration, reaches the cord by way of thicker, myelinated A-delta fibers. Dull, aching, burning pain, longer in duration and slower in onset, travels along smaller, nonmyelinated C fibers. When the pain signal reaches the dorsal horn, various neurotransmitters activate spinal neurons that send axons across the spinal cord and up fiber tracts that eventually reach the medulla, midbrain, and thalamus. From the thalamus, neurons project to the prefrontal cortex, the motor cortex, the somatosensory cortex, the limbic system, and the hypothalamus. Pain information also finds its way to the pons, cerebellum, and basal ganglia through pathways that remain to be fully elucidated. Besides the modulation that can be brought about during the ascent of pain signals, descending inhibitory pathways activated in the midbrain, brainstem, and numerous other areas (among them the amygdala, the hypothalamus, the arcuate nucleus, and the periaqueductal gray matter) can modify the transmission of these impulses. PNT aims to influence the balance within this very complex network, enhancing the inhibitory drives and suppressing the excitatory message. The transmission of pain signals throughout these pathways depends on the balance of neurotransmitters whose release depends, in turn, on a variety of factors, including the frequency of stimulation of the peripheral nerves. Rather than reviewing the various forms of gate theory, originally proposed by Melzack and Wall,1 we will focus here on the influence of different frequencies of electrostimulation on neurotransmitter release in the central nervous system because this neuromodulation underlies the therapeutic effectiveness of PNT. Much of this knowledge derives from electroacupuncture and neurosurgery research, as noted earlier. Early work by Han and colleagues from Beijing Medical University demonstrated that analgesia induced by electroacupuncture of different frequencies is mediated by different opioid receptors.2 131

132  Complementary and Alternative Medical Procedures

Analgesia induced by low-frequency (2 Hz) electroacupuncture resulted from activation of mu- and delta-opioid receptors, whereas analgesia induced by high-frequency (100 Hz) electroacupuncture derived from activation of kappa-opioid receptors. Intermediate frequency stimulation (2 to 15 Hz) activated all three types of receptors in the spinal cord of rats. Further work by Han and colleagues3 showed that lowfrequency (2 Hz) peripheral stimulation produces a significant increase in enkephalin release into the lumbar cerebrospinal fluid (CSF), whereas high-frequency (100 Hz) peripheral stimulation increases dynorphin release. This validated earlier work by Mayer and colleagues4 and Pomeranz and Chiu.5 Wang and associates went on to establish that a more potent analgesia could be established by asynchronous electroacupuncture stimulation—alternating between low-frequency (2 Hz) and high-frequency (100 Hz) stimulation—than could be attained by synchronous electroacupuncture stimulation, combining low and high-frequency stimulation at the same time.6 The clinical application of these findings will become evident later in this chapter. The endorphins (enkephalin and dynorphin) are only part of an ever-elaborating story of pain neurotransmission. In the last few years, research has suggested a role in electroacupuncture (and, thus, PNT) for cocaine and amphetamine-regulated transcript (CART) peptide,7 arginine vasopressin,8 serotonin, catecholamine, and spinal Fos expression,9 interleukin-1-beta,10 corticotrophinreleasing hormone.11 No doubt more neurotransmitters and neurochemicals will play important parts in the transmission and perception of pain. In summary, pain perception is complex and incompletely understood. How PNT modulates the perception of pain remains unclear. Nevertheless, based on this knowledge from basic research and the principles realized through careful clinical study, PNT can be used effectively to address a broad range of chronic painful conditions.

The PNT Technique In a typical treatment session, ten 32-gauge stainless steel acupuncture needles are inserted to a depth of 2 to 4 cm into the soft tissues and/or paraspinous muscles in and around the dermatomal distribution that covers the painful site(s). The 10 needle probes are then connected to five bipolar leads, with each lead connected to one positive and one negative probe in a pattern designed to direct the stimulus along the path of the nerve supplying the dermatome. The probes are then stimulated at an alternating frequency of 15 Hz and 30 Hz for 30 minutes, with the intensity of the stimulation adjusted to produce a gentle tapping sensation without muscle contraction. Treatment sessions can occur once to several times per week. In published trials, treatments have ranged from 2 to 12 weeks, but the overall duration of treatment in the real clinical setting depends on the patient’s response. The details of the typical treatment session have been defined through a number of clinical trials investigating specific aspects of the treatment. Here we will describe research supporting the location of the needle probes, the stimulation montage, the stimulation frequency used, and the duration of electrical stimulation. Location of Needles If the mechanism for analgesia relies primarily on increases in analgesic-like neurotransmitters within the central nervous system induced by peripheral nerve stimulation, varying the level of spinal

stimulation should yield similar analgesic effects. Alternatively, if central neuromodulatory changes are primarily responsible for the analgesic effects, then stimulation of peripheral nerves in or near the affected area should prove more effective than stimulation of distant peripheral nerves. White, Craig, and others clarified the effect of the location of electrical stimulation on the acute analgesic response to PNT in a crossover study of 68 patients with nonradiating neck pain.12 When PNT was applied to needles located in the dermatomal distribution of the neck pain, visual analog pain scores decreased significantly more than when PNT was applied to needles located in the low back region or when needles were inserted without electrical stimulation. PNT applied to local needles also brought significant improvements in physical activity, quality of sleep, psychological wellbeing, and the need for oral analgesic medications, compared with PNT applied to distant needles or unstimulated needles. Moreover, unlike the other two treatments, PNT with the local needles showed a cumulative improvement over the course of therapy (Fig. 16-1). At least in patients with neck pain, therefore, electrical stimulation at the dermatomal levels corresponding to the local pathology provides a greater analgesic effect than does stimulation at remote dermatomes, and electrical stimulation is required to provide the optimal hypoalgesic effect. In order for PNT to be most effective, the practitioner must identify the dermatomes that overlap and surround the painful area and place the needle probes within these dermatomes. Stimulation Montage Having placed the needles into the appropriate dermatomes, does it matter how one connects the stimulator leads? In other words, does one specific pattern of electrical stimulation (i.e., montage) provide greater relief than another specific pattern? Work by White and associates demonstrates that montage matters.13 The investigators evaluated the effect of four different montages on the acute analgesic response to PNT when applied at the same dermatomal levels in a crossover study of 72 patients with low back pain (Fig. 16-2). Although all four montages provided significant improvements in pain visual analog scores and in the physical component summary (PCS) and the mental component summary (MCS) of the SF-36, one montage—in which the flow of electrical stimulation paralleled the dermatomes on both sides—produced significantly greater improvements. The cumulative effects over the course of 2 weeks of treatment were also superior with this montage than with the other patterns. The researchers speculated that the stimulation pattern used with this montage produced more effective electrical stimulation of the involved myotomes and/or sclerotomes and concluded that this montage should be employed in the initial treatment. If this pattern fails, however, they advised resorting to another montage. When initiating PNT, therefore, the best montage employs needles within and around the affected dermatome and electrical stimulation bilaterally between needles in the same dermatome. Stimulus Frequency From the animal and human data already described, it would appear that stimulus with alternating frequencies should afford greater pain relief than stimulus with a single frequency. Ghoname and colleagues tested this hypothesis by comparing the effect of three different frequencies on the analgesic response to PNT therapy in 68 patients with low back pain resulting from degenerative lumbar disc disease. Patients were treated with PNT therapy at 4 Hz, alternating

Percutaneous Neuromodulation Therapy  133 Local dermatomal insertion sites

Remote dermatomal insertion sites

+ − − + + − − + +

− T12

+ − L − L12 + L + L34 − L5

− S1 + S2 S3

+

A

−

B

Figure 16-1  A, The location of the needle electrodes for the “needles only” (control) and the local dermatomal stimulation treatments. With local dermatomal stimulation therapy, each of the five bipolar leads from the stimulation device was connected to a pair of needles, alternation the positive (+) and negative (−) connectors as shown. B, The location of the needle electrodes for the remote dermatomal stimulation treatment sessions, with each of the five bipolar leads from the stimulation device connected to a pair of needles, alternating the positive (+) and negative (−) connectors. (Adapted from White PF, Craig WF, Vakharia AS, et al: Percutaneous neuromodulation therapy: Does the location of electrical simulation effect the acute analgesic response? Anesth Analg 2000;91:949-954.)

3-second pulses of 15 Hz and 30 Hz, and 100 Hz, as well as shamPNT (0 Hz), in random order, three times weekly for 2 weeks, with 1 week off between each sequence. All three frequencies (4 Hz, 15/30 Hz, and 100 Hz) produced significant decreases in pain scores immediately after the treatment and over the 2-week treatment period, as well as significant improvements in physical activity, sleep quality, and need for oral analgesic medications. The overall improvements were significantly greater after 15/30 Hz PNT than after 4 Hz or 100 Hz PNT. During the 15/30 Hz sequence, patients reported significantly greater improvements in their sense of well-being, compared with the other sequences, and more patients preferred the 15/30 Hz therapy (40%) than preferred the 4 Hz (28%), 100 Hz (30%), or sham (2%) treatments.

Whereas these findings led to the adoption of using a mixed frequency (in this case, alternating 15 Hz and 30 Hz with the stimulation pulses switched on and off every 3 seconds), the optimal combination of frequencies may vary with different patients. The important conclusion is that low and high frequencies in tandem likely stimulate a more diverse mix of inhibitory neurotransmitters than does either the use of a single frequency or the simultaneous application of more than one frequency. PNT using a pair of frequencies applied asynchronously provides optimal pain relief. Duration of Electrical Stimulation The needles should be placed within and around the affected dermatome, the stimulus should be applied pair-wise to needles within a single dermatome, and the stimulus should consist of two

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+ TL12 − 1 − L2 + L3 L + 4 − L5

−

− S1 + S2 S3 +

A

B

Montage I

− + − +

C

T12 L1 L2 L3 L4 L5 S1 S2 S3

−

Montage II

+

−

−

+ − +

+

−

Montage III

+

− S1 + S2 S3 +

−

+

− TL12 + 1 L2 L3 + L − 4 L5

D

−

T−12 L1 + − L2 L3 L4 L5 +1 S S2 S3

−

+

Montage IV

Figure 16-2  The needle insertion positions and electrode pairing patterns used for the four different PNT montages. Montage I (A) was the standard montage used in all of the earlier PNT studies involving patients with low back pain. (Adapted from White PF, Ghoname EA, Ahmed HE, et al: The effect of montage on the analgesic response to percutaneous neuromodulation therapy. Anesth Analg 2001;92:483-487.)

f­ requencies (one higher, one lower) used asynchronously. But how long should the electrical stimulation last? Hamza and coworkers addressed this question in a crossover study of 75 patients with low back pain.14 All patients received electrical stimulation for 0, 15, 30, or 45 minutes in a randomized sequence over the course of an 11-week period (2 weeks of treatment with 1 week off between treatments). The researchers

assessed pain scores, health status, sleep quality, and daily oral analgesic requirements. Electrical stimulation for 15, 30, and 45 minutes significantly improved all measures of pain relief over results obtained with 0 minutes of electrical stimulation. After completion of the sixth treatment, mean improvements in the degree of pain, physical activity, and sleep quality and reductions in the need for oral

Percutaneous Neuromodulation Therapy  135

analgesics were significantly greater with 30- and 45-minute treatment intervals than with the 15-minute treatment interval. Improvements in the physical and mental components of the health survey (SF-36) were greater after the 30-minute interval than after the 45-minute interval, but the differences did not reach statistical significance. Clearly, however, adding 15 minutes afforded no improvement over the 30 minutes of electrical stimulation. These findings support the use of 30 minutes of PNT, at least in patients with low back pain.

Clinical Applications of PNT PNT has been used by Craig and others for a host of chronic pain applications. Research to support the use of PNT, however, is sparse. What follows is a selection of indications for PNT, each supported by at least one clinical trial demonstrating efficacy.

Back Pain Back pain, especially low back pain, is one of the most common medical problems, with about 25% of Americans reporting at least one whole day of low back pain in any given 3-month period.15 Despite this high prevalence of back pain, analgesic therapy remains largely unsatisfactory, and controversy surrounds the effectiveness of such nonpharmacologic therapies as transcutaneous electrical nerve stimulation (TENS), acupuncture, spinal manipulation, and exercise therapy. At least five reports have demonstrated PNT to be safe and effective therapy for low back pain. Ghoname and colleagues compared the effectiveness of PNT, sham-PNT (needle placement without electrical stimulation), TENS, and flexion-extension exercise therapies in a randomized, crossover study of 29 men and 31 women with at least 3 months of low back pain secondary to degenerative disc disease.16 Each treatment was administered for 30 minutes three times weekly for 3 weeks. Patients had 1 week without therapy between each of the treatments. PNT in this study used a uniform electrical stimulation frequency of 4 Hz. The principal outcome measures included preand posttreatment visual analog scale (VAS) scores for pain, physical activity, and quality of sleep; daily analgesic medication usage; a global patient assessment questionnaire; and Health Status Survey Short Form (SF-36). PNT produced significantly greater improvements in the PCS and MCS components of the SF-36, compared with TENS, shamPNT, and flexion-extension exercise. PNT improved VAS scores by 46%, physical activity scores by 42%, and sleep quality scores by 44%, whereas TENS improved pain scores by 11% and physical activity scores by 15%. PNT therapy was associated with a 50% reduction in the daily oral analgesic requirement. In comparison, TENS therapy decreased the need for analgesic medication on only 6 days of the 3-week study period. Neither sham-PNT nor exercise therapy provided significant pain relief or altered usage of oral analgesic medication. PNT produced an acute analgesic effect immediately after each treatment session, and patients began reporting significant improvements in their pain, activity, and sleep after three to four treatment sessions. In the overall evaluation of treatments, 91% of patients preferred PNT, 7% preferred TENS, 2% preferred shamPNT, and none preferred exercise. Weiner and associates compared the efficacy of combined PNT and physical therapy (PT) with that of combined sham-PNT

and PT for the treatment of chronic low back pain (defined as that occurring daily or almost every day for the previous 3 months) in a randomized, controlled trial of 34 community-dwelling adults aged 65 years and older.17 Patients received PNT or sham-PNT plus physical therapy twice weekly for 6 weeks. These investigators used a structured PNT protocol that allowed incremental stimulation frequencies based on the patient’s response to therapy. The primary outcome measures were pain intensity and pain-related disability, and secondary outcome measures included physical performance, psychosocial factors, and cognitive function. Unlike the sham-PNT plus PT group, the PNT plus PT group showed significant reductions in pain intensity measures from pre- to posttreatment. The improvements in pain intensity were sustained from posttreatment to the 3-month follow-up visit. Painrelated disability also declined significantly in the PNT plus PT group but did not improve in the sham-PNT plus PT group. The PNT plus PT group experienced consistent improvements in physical performance and psychosocial functioning, whereas the sham-PNT plus PT group experienced few improvements in physical performance and no significant changes in psychosocial functioning. Neither treatment was associated with significant changes in cognitive performance. Low back pain is also prevalent in Taiwan, affecting some 80% of the population at some point during their lives. Hsieh and colleagues from National Taiwan University, Taipei, Taiwan investigated the therapeutic effects of one-shot, low-frequency PNT plus medication versus one-shot TENS plus medication or medication only in 133 patients with low back pain. Just over half the patients (56%) had acute low back pain, 20% had subacute low back pain, and 24% had chronic low back pain. Both PNT and TENS employed alternating 3 Hz and 15 Hz stimulation pulses for a total of 15 minutes in a single session. Outcome measures included pain VAS score, body surface score, pain pressure threshold, and the Quebec Back Pain Disability Scale. PNT and TENS were associated with significant improvements in pain VAS score and body surface score immediately after the one-shot treatments. By 1 week after treatment, the improvements in pain scores and body surface scores did not differ among PNT, TENS, and medication-only groups. Pain pressure threshold did not improve immediately after treatment, and improvements at 1 week posttreatment did not differ among the groups. Quebec Back Pain Disability Scores were most improved after PNT, but the differences among the groups were not significant immediately after treatment or 1 week later. The investigators concluded that one-shot PNT (or TENS) provides only temporary relief of back pain. Borg-Stein and associates extended the use of PNT to the management of subacute radiating low back pain.18 They investigated the efficacy and safety of 12 weeks of weekly PNT for 30 minutes in an open-label study of 59 patients who had moderate-to-severe radiating low back pain for 4 weeks to 6 months. According to their report, the pulse repetition frequency varied from 4 Hz to 10 Hz in a periodic, sweeping manner. Their outcome measures included VAS scores of radiating pain, low back pain, physical activity, and sleep, as well as the Oswestry Disability Questionnaire. By the 5-week evaluation, 37 patients (63%) reported at least a 30% decrease in their lower extremity pain and 25 patients (42%) reported at least a 50% improvement. Among all 59 patients, mean leg/buttock pain decreased by 37%, mean low back pain decreased by 26%, activity levels improved by 38%, sleep improved by 27%, and Oswestry Low Back Pain Disability scores

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improved by 24%. These improvements were sustained between 5 and 12 weeks. By 24 weeks, 83% of 27 patients who granted phone interviews indicated either “very much benefit” or “much benefit,” and 59% said they were either “pain free” or “much better.” Yokoyama and colleagues from Okayama University Medical School, Okayama City, Japan compared PNT with TENS for longterm pain relief in a study of 60 patients who reported having low back pain with intensity of at least 40/100 on VAS for more than 6 months.19 One group received PNT twice weekly for 8 weeks, one group received 4 weeks of twice-weekly PNT followed by 4 weeks of twice-weekly TENS, and one group received 8 weeks of twiceweekly TENS. In all cases, needles or TENS electrode pads were stimulated with alternating frequencies of 4 Hz and 30 Hz for 20 minutes. Pain level, degree of physical impairment, and daily intake of nonsteroidal antiinflammatory drugs (NSAIDs) were assessed 3 days after week 2, week 4, and week 8 treatments and again at 1 and 2 months after the sessions concluded. VAS pain scores improved significantly at 2 weeks, 4 weeks, 8 weeks, and at the 1-month post-treatment follow-up in the group treated with 8 weeks of PNT. By the 2-month follow-up, pain scores had returned to pretreatment values. Similarly, VAS pain scores improved significantly at 2 weeks, 4 weeks, and 8 weeks in the PNTTENS group, but scores had returned to pretreatment values by the 1-month and 2-month follow-up assessments. Only the 8-week pain scores were improved in the group that had 8 weeks of TENS. Peak pain scores were lowest in the group treated with 8 weeks of PNT; intermediate in the group that received 4 weeks of PNT followed by 4 weeks of TENS; and highest in the group that received 8 weeks of TENS. Findings were similar for the degree of physical impairment and the daily intake of oral NSAIDs. Taken together, these studies demonstrate that PNT can provide relief of pain, improved physical functioning, improved sleep, and decreased need for oral analgesics in patients with chronic low back pain (with or without radiating pain). Because most of these studies have not taken advantage of the fine-tuning granted by the research described earlier (especially regarding montage and asynchronous frequency electrical stimulation), it is likely that greater improvements in pain, functioning, and quality of life can be realized in these patients.

Sciatica As many as 40% of people experience sciatica (radicular pain in the distribution of the sciatic nerve caused by herniation of one or more lumbar intervertebral discs) in their lifetime.20 Ghoname and coworkers compared PNT, sham-PNT, and TENS for the management of the radicular pain in a crossover study of 64 patients with sciatica due to radiologically-confirmed lumbar disc herniation. PNT and TENS (applied only to the affected leg) employed a stimulation frequency of 4 Hz during 30-minute sessions three times weekly for 3 weeks. All patients received all three modalities, and each set of treatments was separated by a 1-week period free of therapy. The primary outcome measures were the pain VAS and the SF-36. Secondary outcomes included physical activity, sleep quality, sense of well-being, and daily oral analgesic requirements. PNT provided the greatest improvements in the physical and mental components of the SF-36, although both TENS and shamPNT produced significant improvements in the scores. Similarly, the average decreases in VAS pain scores immediately after treatment and 24 hours after the last treatment session were significantly greater after PNT than after TENS or sham-PNT. PNT also

produced significant improvements in VAS scores for activity and sleep after three to four treatments, as did TENS (but to a lesser degree). The improved sense of well-being and decrease in daily oral analgesic requirements were most significant after PNT. In the overall evaluation by patients, nearly three-quarters preferred PNT (73%), compared with 21% who preferred TENS, and 6% who preferred sham-PNT. Most patients indicated a willingness to pay extra money to receive PNT therapy in the future. Although more research is needed to determine what factors contribute to successful treatment, PNT shows promise as a treatment for patients with sciatica.

Neuropathic Pain Peripheral neuropathy may complicate the course of diabetes in as many as 47% of patients, and more than 26% of diabetics have reported experiencing pain or tingling.21 Various drug classes have been employed in an effort to ameliorate neuropathic pain, and nonpharmacologic approaches—TENS, acupuncture, and spinal cord stimulation—have afforded some relief. Hamza and coworkers evaluated the effectiveness of PNT in the management of diabetic neuropathic pain in a crossover study of 50 adult patients with longstanding type 2 diabetes and peripheral neuropathic pain. Patients were treated in random order with PNT and sham-PNT for 30 minutes three times weekly for 3 weeks, with 1 week “off ” between treatments. During PNT, needles were stimulated with alternating frequencies of 15 Hz and 30 Hz; the needles were not stimulated during sham-PNT. Outcome measures included VAS scores, SF-36 scores, oral analgesic medication requirements, the Beck Depression Inventory (BDI), and the Profile of Mood States (POMS), and a patient preference questionnaire. VAS scores for extremity pain, physical activity, and sleep quality improved significantly after PNT, but did not change after sham-PNT. PNT and sham-PNT produced significant improvements in the physical and mental component scores of the SF-36, although the improvements were significantly greater after PNT than after sham-PNT. Similarly, improvements in the BDI scores and on all POMS measures were significantly greater after PNT than after sham-PNT. During PNT, patients reduced their daily oral nonopioid analgesic medication by 49%, whereas during shamPNT the reduction (14%) did not attain statistical significance. The post-study evaluation indicated that 92% of patients preferred PNT over sham-PNT, 88% reported an improved sense of well-being after PNT, and 92% expressed a willingness to pay extra money for PNT in the future. PNT appears safe and effective for the treatment of diabetic neuropathic pain. Although it does not provide complete relief, it can improve quality of life and reduce the need for oral analgesic medication. More research is needed to determine its optimal role in the management of these patients.

Bone Pain Carcinomas of the breast, prostate, kidney, lung, and thyroid commonly metastasize to bone, where pain is the most common symptom. Large doses of opioids often provide inadequate relief and bring undesirable sedation and gastrointestinal side effects. Nonpharmacologic alternatives to analgesic medication have been considered, but results with TENS have been disappointing. Ahmed and associates evaluated the use of PNT for the shortterm management of pain associated with metastatic cancer in a

Percutaneous Neuromodulation Therapy  137

pilot study of three patients whose symptoms were inadequately controlled with conventional opioid and nonopioid analgesics.22 The first patient, a 76-year-old Hispanic man with prostate cancer metastatic to the spine, received PNT with needles inserted into the periosteum (negative electrode) and soft tissue (positive electrode) bilaterally at the level of T10, T12, and S1. The needles were stimulated alternately at 15 Hz and 30 Hz for 30 minutes. Pain diminished from 7/10 to 2/10 (per visual analog pain scale) immediately after treatment but rebounded to 5.5/10 three days later. A second treatment reduced the pain to a level manageable by oral analgesic medication. The second patient, a 51-year-old black man with rectal carcinoma metastatic to the sacral region, underwent PNT with needles inserted into the periosteum and soft tissue bilaterally at the level of T12, L4, and S1. These needles were stimulated at an initial frequency of 6 Hz for 30 minutes. Immediately after treatment, VAS pain scores fell from 9/10 to 2/10. Pain rebounded days later, and he received several additional successful PNT sessions before being referred to a neurosurgeon who implanted a dorsal column stimulator that allowed him to maintain his pain at a tolerable level, requiring only occasional use of an oral NSAID or an NSAID/opioid combination. The third patient was a 78-year-old retired white man with gallbladder cancer with local tumor extension, but no evidence of bony metastases. He received three consecutive PNT treatments for uncontrolled pain in the right upper quadrant radiating through to his back at the level of T6 to T8. Again, a combination of periosteal and soft tissue needles at T4, T10, and T12 was stimulated at 4 Hz, alternating 15 Hz/30 Hz, and 100 Hz, respectively. The patient obtained no significant relief of his pain symptoms, and PNT was discontinued. Although these results are clearly preliminary, PNT may have a role in the palliative management of pain associated with bony metastases from solid cancers. Further studies will be needed to determine its exact role.

Other Possible Indications for PNT Craig and many others have personally reported the effectiveness of PNT in addressing a variety of medical conditions, mostly in the form of anecdotes recounted during workshops or informal presentations. Two published reports have discussed the use of PNT for headaches induced by electroconvulsive therapy and for the pain associated with acute herpes zoster infection. Ghoname and colleagues used PNT to treat five patients who experienced migraine-like attacks associated with electroconvulsive therapy (ECT).23 The first patient obtained relief from a severe, bilateral, throbbing headache that developed after ECT after receiving 30 minutes of PNT delivered at 4 Hz through needle probes placed bilaterally in the temporalis muscles and the paraspinous muscles at dermatomal levels C1, C5, C7, and T4. Based on this result, the investigators administered PNT for 30 minutes prior to the induction of anesthesia for the patient’s next ECT treatment. The patient remained headache-free after this ECT session. Because of their success with the first patient, the researchers applied pre-ECT PNT with success in four additional patients. In all cases, the patients experienced complete or partial freedom from post-ECT headaches. Sham-PNT (identical needle placement without electrical stimulation) in all five patients failed to provide headache relief or to prevent the development of post-ECT headache. As noted by these authors, randomized, controlled trials will be required to confirm these results and to determine the relative

efficacy of PNT and other therapies (including serotonin antagonists) for preventing ECT-evoked headaches. Antiviral drugs have been employed successfully to decrease the pain and enhance the resolution of acute herpes zoster lesions in immunocompetent patients, but their effects on postherpetic neuralgia (PHN) remain controversial. Ahmed and colleagues compared the effects of PNT with those of a standard antiviral regimen on pain, physical activity, sleep quality, cutaneous lesion resolution, and incidence and severity of PHN in 50 adult patients with the onset of herpes zoster lesions within the preceding 72 hours.24 The patients were randomized to receive either famciclovir 500 mg three times daily for 1 week or PNT for 30 minutes three times weekly for 2 weeks. The needles for PNT were inserted at dermatomes one level above and one level below the cutaneous lesions and were stimulated at frequencies ranging from 4 Hz to 100 Hz. Patients treated with PNT experienced clearing of vesicles 1 day earlier and healing of cutaneous lesions 2 days earlier than did patients treated with famciclovir. PHN VAS scores at 3 months and 6 months after treatment were significantly lower in the PNT group (32/100 and 30/100, respectively) than in the famciclovir group (44/100 and 46/100, respectively). By 9 months after treatment, the difference in PHN VAS was no longer significant (49/100 after PNT versus 55/100 after famciclovir). After 2 weeks of treatment, PNT patients had significantly better pain, activity, and sleep scores than patients treated with famciclovir. Although it is unlikely to supplant antiviral drugs as the firstline therapy for patients with acute herpes zoster, PNT may offer an important complement to antiviral therapy.25 More research is needed to elucidate the role of PNT in this painful condition.

Conclusion Over the past 30 years, Craig and others have refined PNT into a safe and effective approach to managing a broad range of painful conditions. PNT has demonstrated effectiveness for low back pain with or without radiation, sciatica, diabetic neuropathic pain, metastatic bone pain, and other disorders, and there are no reports of significant complications associated with the procedure. Patients tolerate PNT well and express a preference for PNT over other nonpharmacologic approaches to pain management. PNT is easy to learn and straightforward to apply in a variety of settings. Practitioners should consider using PNT as primary or complementary treatment for patients presenting with pain refractory to other treatments. The first step after a complete diagnostic assessment is the identification of the painful dermatome, myotome, or sclerotome. Unless precluded by cutaneous lesions, needles should be placed in the affected dermatome and in dermatomal levels that surround the affected dermatome. Electrical stimulation should employ alternating low and high frequencies during sessions lasting 30 minutes or more for best results. The number of sessions (weekly and overall) will necessarily depend on the condition under treatment, the schedule of the patient, and the effectiveness of the treatment. For some conditions, a few sessions of PNT will bring permanent and total pain relief. Other conditions may require indefinite PNT in combination with other modalities to provide optimal pain amelioration. When PNT affords no relief, it should be abandoned in favor of other therapeutic approaches. Future studies should explore different montages and frequency combinations for different painful conditions. Although the duration of a treatment session has been studied, the frequency

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of treatment and the overall duration of a program of treatment demand further investigation. How long the beneficial effects of PNT can be expected to persist also requires additional study. In the meantime, PNT can be practiced safely and effectively for chronic pain using the parameters described here. PNT should be added to the therapeutic armamentarium of all practitioners who care for patients with chronic pain. REFERENCES   1. Melzack P, Wall PD. Pain mechanisms: A new theory. Science. 1965;150:971-979.   2. Chen XH, Han JS. Analgesia induced by electroacupuncture of different frequencies is mediated by different types of opioid receptors: Another cross-tolerance study. Behav Brain Res. 1992;47:143-149.   3. Han JS, Chen XH, Sun SL, et al. Effect of low- and high-frequency TENS on Met-enkephalin-Arg-Phe and dynorphin A immunoreactivity in human lumbar CSF. Pain. 1991;47:295-298.   4. Mayer DJ, Price DD, Rafii A. Antagonism of acupuncture analgesia in man by the narcotic antagonist naloxone. Brain Res. 1977;121:368-372.   5. Pomeranz B, Chiu D. Naloxone blocks acupuncture analgesia and causes hyperalgesia: Endorphin is implicated. Life Sci. 1976;19:1757-1762.   6. Wang Y, Zhang Y, Wang W, et al. Effects of synchronous or asynchronous electroacupuncture stimulation with low versus high frequency on spinal opioid release and tail flick nociception. Exp Neurol. 2005;192:156-162.   7. Tian DR, Li XD, Wang F, et al. Up-regulation of the expression of cocaine and amphetamine-regulated transcript peptide by electroacupuncture in the arcuate nucleus of diet-induced obese rats. Neurosci Lett. 2005;383:17-21.   8. Yang J, Liu WY, Song CY, Lin BC. Only arginine vasopressin, not oxytocin and endogenous opiate peptides, in hypothalamic paraventricular nucleus play a role in acupuncture analgesia in the rat. Brain Res Bull. 2006;68:453-458.   9. Li A, Wang Y, Xin J, et al. Electroacupuncture suppresses hyperalgesia and spinal Fos expression by activating the descending inhibitory system. Brain Res. 2007;1186:171-179. 10. Zhang RX, Li A, Liu B, et al. Electroacupuncture attenuates bone cancer pain and inhibits spinal interleukin-1-beta expression in a rat model. Anesth Analg. 2007;105:1482-1488. 11. Li A, Lao L, Wang Y, et al. Electroacupuncture activates corticotrophinreleasing hormone-containing neurons in the paraventricular nucleus of the hypothalamus to alleviate edema in a rat model of inflammation. BMC Complement Altern Med. 2008;8:20.

12. White PF, Craig WF, Vakharia AS, et al. Percutaneous neuromodulation therapy: Does the location of electrical stimulation effect [sic] the acute analgesic response? Anesth Analg. 2000;91:949-954. 13. White PF, Ghoname EA, Ahmed HE, et al. The effect of montage on the analgesic response to percutaneous neuromodulation therapy. Anesth Analg. 2001;92:483-487. 14. Hamza MA, Ghoname EA, White PF, et al. Effect of the duration of electrical stimulation on the analgesic response in patients with low back pain. Anesthesiology. 1999;91:1622-1627. 15. Deyo RA, Mirza SK, Martin BI. Back pain prevalence and visit rates: Estimates from U.S. national surveys, 2002. Spine. 2006;31:2724-2727. 16. Ghoname EA, Craig WF, White PF, et al. Percutaneous electrical nerve stimulation for low back pain: A randomized crossover study. JAMA. 1999;281:818-823. 17. Weiner DK, Rudy TE, Glick RM, et al. Efficacy of percutaneous electrical nerve stimulation for the treatment of chronic low back pain in older adults. J Am Geriatr Soc. 2003;51:599-608. 18. Borg-Stein J, Seroussi RE, Gomba L, et al. Safety and efficacy of percutaneous neuromodulation therapy in the management of subacute radiating low back pain. Pain Practice. 2003;3:125-134. 19. Yokoyama M, Sun X, Oku S, et al. Comparison of percutaneous electrical nerve stimulation with transcutaneous electrical nerve stimulation for long-term pain relief in patients with chronic low back pain. Anesth Analg. 2004;98:1552-1556. 20. Stafford MA, Peng P, Hill DA. Sciatica: A review of history, epidemiology, pathogenesis, and the role of epidural steroid injection in management. Br J Anaesth. 2007;99:461-473. 21. Barrett AM, Lucero MA, Le T, et al. Epidemiology, public health burden, and treatment of diabetic peripheral neuropathic pain: A review. Pain Med. 2007;8S2:S50-S62. 22. Ahmed HE, Craig WF, White PF, Huber P. Percutaneous electrical nerve stimulation (PENS): A complementary therapy for the management of pain secondary to bony metastasis. Clin J Pain. 1998;14:320-323. 23. Ghoname EA, Craig WF, White PF. Use of percutaneous electrical nerve stimulation (PENS) for treating ECT-induced headaches. Headache. 1999;39:502-505. 24. Ahmed HE, Craig WF, White PF, et al. Percutaneous electrical nerve stimulation: An alternative to antiviral drugs for acute herpes zoster. Anesth Analg. 1998;87:911-914. 25. Dworkin RH. No alternative to antiviral drugs for acute herpes zoster [letter]. Anesth Analg. 1999;89:1585-1586.

Medical Acupuncture

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Aram Mardian, MD

In the decade since the publication of the National Institutes of Health (NIH) white paper on acupuncture in 1997, peer-reviewed, responsible research into the mechanism and efficacy of acupuncture has been prolific. As this research has identified acupuncture as a safe, efficacious, and cost effective modality to treat a variety of pain problems, it is in the process of being gradually integrated into the field of conventional pain medicine.

Brief History Acupuncture is a complex therapeutic process that has its roots in prehistory and is undergoing constant evolution as its use in the conventional modern healthcare setting expands and understanding of its mechanism grows. Now, having existed for almost forty years in the public consciousness of the general population of the United States and scientific community, there is considerable familiarity with the basics of acupuncture as a therapeutic modality. Most are aware that acupuncture is the use of thin, solid needles in various patterns on the body. Although this is taken for granted in 21st century America, prior to July 26, 1971, outside of Asian communities, acupuncture was a wholly unknown entity in the United States. On that date, James Reston’s landmark article describing his experience with acupuncture in China was published in The New York Times.1 Mr. Reston was a reporter for the “Times” who had traveled to China in 1971 in preparation for Richard Nixon’s historic diplomatic visit. Mr. Reston required an emergency appendectomy in Peking and had his postappendectomy pain successfully treated with acupuncture. This experience was recounted to the American people in The New York Times publication and served as the first major exposure of the English speaking U.S. population to acupuncture. Shortly after Nixon’s trip, physicians began formal and informal trips to China where they witnessed surgical anesthesia using only acupuncture needles. Whereas Reston’s article ignited popular interest in acupuncture, these reports began to fuel curiosity in the medical and scientific communities and served to spark scientific exploration of the bizarre “new” technique. As the specifics of the endorphin theory of acupuncture analgesia were discovered in the late 1970s, respect within the scientific community grew proportionately. While likely practiced for several thousands of years BCE, the first known text that formally describes acupuncture theory is Huang Di Nei Jing (Yellow Emperor’s Classic of Medicine), which dates to the 2nd century bc. A more comprehensive text with greater unification of acupuncture theories was written in the

first and second centuries ad and was called the Nan Jing (Classic of Difficult Issues). By this time, most of the concepts that underlie classical acupuncture theory such as acupuncture point location, channels, and disease classification had been defined. Transmission of knowledge occurred largely along familial lines in China leading to a multitude of diverse ways of practicing acupuncture. From the 2nd century ad to the 16th century ad, these theoretical concepts and the practical application of acupuncture underwent an extensive and continual refinement that typifies the empirical evolution of this system of treatment. These refinements and the current state of acupuncture theory and practice were captured in the Zhen Jiu Da Cheng (Great Compendium of Acupuncture and Moxibustion) which is attributed to Yang Ji-Zhou and was published in 1601. This text, referred to as the Da Cheng, became the preeminent source for medical information for subsequent generations in Asia and Europe. In fact, it was this text that was translated into various languages and transmitted to Europe and Japan by traveling physicians and missionaries from the 1600s through the 1900s and served as the basis for the development of classical acupuncture in these regions. The practice of acupuncture and herbal medicine experienced a dramatic decline in China in the first half of the twentieth century. This process was driven by the larger cultural process of modernization patterned after Western science during this same period. Prior to the 19th century, China was the undisputed power that dominated the Eastern Hemisphere. A series of events in the 19th century including the Opium Wars, the Taiping Rebellion, and famine claimed tens of millions of lives and left China politically weakened and at the mercy of Western powers such as the French and the British for the first time in history. Accustomed to military and scientific superiority, the defeat of China by the British in the Opium Wars initiated a cultural drive to quickly adopt the principles of Western science that allowed their military adversaries to prevail. This infatuation with Western military science spilled over into all areas of science including medicine. This devotion to modernization according to Western principles was epitomized in the early 1900s by the repudiation of classical acupuncture and Chinese medicine and a commitment to license only Western-trained physicians. Economic necessity and political expediency led to the simplification and systemization of the variegated forms of classical acupuncture under Mao in the second half of the 20th century in China. After Mao came to power, it became clear that the cadre of newly trained Western physicians, numbering roughly 40,000, was grossly inadequate to care for the more than 500 million Chinese 139

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citizens. Mao’s declaration that “Chinese medicine is a great treasure-house” came in 1958 and served as the theoretical basis for the barefoot doctor movement that was initiated in 1969. During this period, Mao called on previously marginalized practitioners of acupuncture and classical Chinese medicine to create a simplified system of Chinese medicine that could be easily taught and disseminated among his corps of barefoot doctors whose aim would be to care for rural villages. This new system eventually became known as Traditional Chinese Medicine (TCM). Ironically, this system is a 20th century creation and omits many of the complexities and nuances of pre-Mao classical Chinese medicine.2-6 Interestingly, the pre-Mao classical forms of acupuncture find their most authentic preservation outside of China, in Europe, Japan, and America. The Japanese began practicing acupuncture in the 6th century ad and developed unique forms of acupuncture. From its earliest forms in Japan, acupuncture took on distinct qualities. Whereas in China acupuncture was closely combined with herbal medicine, in Japan physical medicine techniques and massage evolved in parallel with acupuncture. Consequently, the acupuncture of Japan requires the careful palpation of subcutaneous and muscular restrictions and nodules. Because of this, Japanese acupuncture has found an easy marriage with physical medicine techniques in modern ­America such as osteopathic manipulation and Janet Travell’s trigger point therapy. The greater freedom enjoyed by modern Japanese society when compared to modern China afforded an environment more amenable to continued evolution and integration with other modern medical practices. Primitive experimentation with acupuncture began in Europe during the early 19th century as translations of the Da Cheng reached England, France, and Germany via military and missionary physicians returning from China. More serious integration with modern Western medicine did not occur until the middle of the 20th century in Europe and later in the United States.2

Acupuncture is not Monolithic It is important to realize that acupuncture is a general term that subsumes many specific techniques. Rather than thinking of acupuncture as a monolithic therapy, it may be helpful to think of acupuncture as one would think of the term injection. Injections using lidocaine and placed into an infraspinatus trigger point clearly represent a very different intervention as compared to a transforaminal epidural steroid injection or the intramuscular administration of ketorolac. Acupuncture techniques can be as distinct.

A Brief Primer of Acupuncture Techniques Classical Chinese acupuncture typically involves the insertion of needles into locations on the body that have been empirically defined over thousands of years. Depth of needles insertion is often determined by achieving a characteristic aching or tingling sensation referred to as De Qi. When reference is made to classical or traditional acupuncture points, this generally implies the group of some 360 “principal” points described in ancient times. It is important to realize that classical acupuncturists have also described several thousand additional “extra” acupuncture points. Classical conceptions of acupuncture channels or meridians refer to linear pathways that connect individual acupuncture points. Japanese acupuncture also evolved throughout ancient times and recognizes acupuncture points and channels similar to those

of classical Chinese acupuncture. Japanese acupuncture involves a more refined system of palpation of subcutaneous and muscular tissue and insertion of needles into areas of myofascial restriction determined by this palpation. Depth of needle insertion is characteristically intracuticular and therefore much more superficial than in classical Chinese acupuncture. A branch of Japanese acupuncture, Ryodoraku, describes acupuncture points and channels as shifting anatomic location according to patterns of pathology manifested by individual patients. Interestingly, many of the sham acupuncture protocols in randomized controlled trials (RCTs) use needling techniques identical to Japanese acupuncture. Neuroanatomic acupuncture is a modern acupuncture technique that is characterized by the insertion of needles into points on the body that have a neuroanatomic significance. Points are generally chosen with the aim of stimulating peripheral nerves, neurovascular bundles, fascia, tendons, muscles, ligaments, joints, and richly innervated structures such as the periosteum and interosseus membranes; electrical stimulation of these points is common. Neuroanatomic acupuncture uses classical acupuncture needle techniques according to modern biomedical knowledge. Percutaneous neuromodulation therapy (PNT), also referred to as percutaneous electrical nerve stimulation (PENS), is a specific form of neuroanatomic acupuncture that positions acupuncture needles in soft tissue or muscles to stimulate spinal nerves and peripheral nerves. After a specific neuromusculoskeletal (NMS) diagnosis is made, the spinal nerves that correspond to the dermatome, sclerotome, myotome, and autonomic innervation of the pathologic region are stimulated at a variety of different electrical frequencies in a variety of different patterns. Acupuncture needles are also placed locally and regionally around the pathologic area according to neuroanatomic principles and stimulated with a variety of electrical frequencies. Auricular acupuncture is a microsystem technique that involves the insertion of various types of needles into predetermined points and points with altered bioelectrical conductance on the external ear. As a microsystem, all aspects of the body are postulated to have representation on the external ear in a holographic fashion. Chinese scalp acupuncture (see Chapter 19) is also a microsystem technique and is characterized by the threading of needles along the scalp according to the underlying functional characteristics of the brain.

Medical Acupuncture is the Unification of Classical Acupuncture and Modern Medicine The optimal acupuncture treatment of pain problems requires familiarity with classical acupuncture teachings as well as modern neuromuscular anatomy and neurophysiology. This unique integration of classical and modern knowledge is the exception rather than the rule among acupuncture practitioners. Many nonphysician acupuncturists lack the requisite familiarity and experience with the modern neuroanatomic understanding of pain to optimally treat many pain problems. While classical acupuncture techniques can be quite effective in treating pain, an approach that does not include the intentional integration of modern neuroanatomic concepts is suboptimal. Among physicians who practice acupuncture, this integrated approach is the ideal, but also not the rule. Some physicians obtain training only in modern neuroanatomic techniques, and this is also a suboptimal approach to pain problems. Medical acupuncture is the practice of acupuncture by physicians; as a discipline it represents the integration of classical acupuncture with modern medicine. Medical acupuncture has

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evolved since the middle of the 19th century initially in Western Europe, then in Japan, and most recently in the United States. It has found its most refined expression in the work of Joseph Helms, MD. Helms has developed a robust and elegant integration of classical acupuncture with diverse modern acupuncture techniques such as neuroanatomic acupuncture, PNT, auricular acupuncture, and scalp acupuncture. It is this integrated system of acupuncture that is referred to by the term medical acupuncture in this chapter.

Medical Acupuncture Education Medical acupuncture is taught to physicians in the United States through continuing medical education courses. The World Health Organization has promulgated acupuncture education standards for physicians and recommends that licensed physicians obtain at least 200 hours of formal training in acupuncture to acquire this specialty medical skill. The American Board of Medical Acupuncture (ABMA) was established in 2000 to promote the safe and efficacious practice of acupuncture by physicians through a standardized examination and certification process. The ABMA is not a member of the American Board of Medical Specialties. The ABMA stipulates requirements for training, experience, and examination. In general, board certification by the ABMA requires 300 hours of formal training in acupuncture, a minimum of 2 years of clinical practice, and passing a standardized written examination. The ABMA currently recognizes 10 training programs in the United States and Canada. The majority of board certified physician acupuncturists have been trained by the Helms Medical Institute, founded by Joseph Helms.

What are the Effects of Medical Acupuncture? As a comprehensive therapeutic system with a variety of techniques, medical acupuncture has wide-ranging effects including pain reduction, improvement in sleep, improvement in anxiety and depression, a reduction in pain medication, improvement in function, and an improvement in energy and vitality.7-13 Conversely, most therapies in conventional medicine have narrowly defined effects such as pain reduction from an epidural steroid injection or improved sleep from a sedative-hypnotic drug. Acupuncture that is used to treat a pain problem can be expected to have multiple effects simultaneously. This is particularly important because many pain problems represent a vicious cycle of pain, dysfunction, psychoemotional disturbances, fatigue, and sleep problems. Part of the robust nature of medical acupuncture is the ability to affect all of these seemingly disparate problems. Medical Acupuncture is More than Needling The practice of medical acupuncture involves therapeutic lifestyle recommendations in addition to needling. Specific dietary suggestions are often combined with prescriptions for exercise or activity modification. Further, classical acupuncture teachings describe an implicit relationship between physical dysfunction and imbalances in the cognitive and emotional spheres. This relationship and the specific areas of psychoemotional imbalances are discussed with the patient. Having a coherent way to understand the relationship between physical and mental imbalances can be enormously helpful for patients. By providing a means for understanding and exploring self-defeating thoughts and behaviors, this system often helps define a path for improving overall self-efficacy.

Medical Acupuncture View of the Human Organism The accumulation of knowledge about human physiology, biochemistry, and pathophysiology within the sphere of modern medicine has been prodigious in the last 50 years. Much of this progress has relied on the ever improving ability to focus on the ever more exact building blocks of the human body. Much of medical therapeutics derives from this scientific process, but also remains incompletely understood. For example, tricyclic antidepressants are effective in treating many chronic pain states and are widely used for this purpose. We know that these medications have many mechanisms of action including the inhibition of presynaptic reuptake of serotonin and norepinephrine as well as blockade of sodium and voltage-dependent calcium channels.14 We do not know, however, the mechanism of action responsible for analgesia,15 nor do we know why some patients respond and others do not. Powerful reductionistic science has identified the mechanisms of these medications and part of the pathophysiology of chronic pain, but will unlikely reveal the unanswered questions of in vivo analgesic mechanisms and individual variability of response. Modern scientific paradigms from modern physics such as systems theory and quantum mechanics will likely be required to propel modern medicine into the next stages of advancement. Scientific approaches to reality require both reductionistic and synthetic processes of investigation. Systems theory is an excellent example of a synthetic scientific approach. Systems theory teaches us that complex systems as primitive as unicellular organisms behave in ways that defy reductionistic, linear laws. Whereas reductionistic models of scientific investigation have proved invaluable for determining many of the components of living systems, this approach to science is suboptimal in providing information about how these components interact in the living organism.16 Systems theory instructs that complex systems, of which the human body is a quintessential example, have emergent properties. Emergent properties are unique properties of complex systems that are not present in any of the more simple parts of the whole, but arise only when all parts interact to form the complex whole. A laudable yet nascent drive in modern medicine is the administration of individualized care. The doctrine of conventional modern medicine is that the specific disease entity must be identified and the pharmaceutical or intervention that is most appropriate to the disease entity must be delivered. That is, all patients with knee osteoarthritis ought to receive the same treatment, all patients with insomnia ought to receive the same treatment, all patients with depression ought to receive the same treatment, and any patient with all three diseases ought to receive all three treatments. Systems theory teaches us that this is a rudimentary approach to the complex system of the human body. First, not all humans with the same disease process will respond the same way to the same treatment. We know that there are individual differences in the pharmacokinetics of medication metabolism and individual differences in the healing process after surgery.17-19 Thus, the best principles of modern science tell us what Dr. Osler told us more than 100 years ago—“It is much more important to know what sort of a patient has a disease than what sort of a disease a patient has.” The goal, then, is individualized approaches that take the complexity of the person’s constitution as well as the disease process into account. The specific science and ability to do this in clinical practice is developing, but still poorly defined. Interestingly, medical acupuncture presents clinicians with an approach that follows these ideals. Part of the nonspecific effects that are attributed to acupuncture’s effectiveness in RCTs may in fact be due to the systematic approach of acupuncture that seeks to

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identify constitutional factors for a patient and individual treatment for a presenting complaint based on that person’s identity and constitution. The classical framework of acupuncture has developed an empirical system that, in essence, looks for emergent properties. Through the thousands of years of empirical observations and subsequent pattern definition, acupuncture has sought to answer the following types of questions: What unique characteristics arise when a person complaining of knee pain also is a competitive, hard driving, leader without other medical problems, versus an overweight, jovial man who also suffers from chronic, debilitating allergic rhinitis? While the conventional approach to treating knee pain in these two patients would be identical, with likely variable results, the acupuncture approach for each would be unique, likely with good results based on large RCTs.20,21 Most of these aspects of acupuncture have not been explored from the perspective of conventional science such as RCTs and are largely speculative. However, such factors, which have been derived from millennia of careful observation and inductive reasoning, may provide insight into the efficacy of acupuncture observed in clinical trials and may lead to new theories that will further reveal the myriad of unknown mechanisms in the functioning of the human body in health and disease. Medical Acupuncture and the Treatment of Complex Chronic Pain Medical acupuncture is a versatile modality that interacts with psychological, neurologic, endocrine, immunologic, and musculoskeletal aspects of the human organism.22-27 With these multiple points of input, medical acupuncture is ideally suited for the treatment of pain, which by nature manifests in the psychoneuromusculoskeletal sphere of humans. The human organism is viewed as a complex multidimensional and integrated whole by physician acupuncturists. This view contrasts with that typically held by conventional pain medicine physicians. Conventional medicine is generally satisfied with dissecting an organism or molecule down to its smallest part and assuming that it understands the functioning of the organism when it has understood the functioning of all of its parts. In conventional clinical pain medicine, we are generally looking for one of a relatively few pain generators, such as a herniated nucleus pulposus or degenerated cartilaginous surface. As such, the biomedical model of pain seeks to identify and treat the physical pain generator that is assumed to be the sole cause of the patient’s pain. Recognition that this approach is inadequate has fostered the development of the biopsychosocial model used to understand and treat pain states. Similarly, medical acupuncture recognizes that many pain problems are a complex manifestation of dysfunction in multiple spheres: myofascial, neurologic, psychological, emotional, endocrine, and genetic. Further, it is recognized that the experience of the organism is greater than the sum of all of these individual spheres. Ronald Melzack recently described a new theory of pain that proposes a similarly complex and multidimensional view of pain problems. It is intriguing that medical acupuncture is capable of influencing virtually all of the components described by Melzack’s new theory of pain.

The Neuromatrix Theory of Pain Consciousness in general and the awareness and experience of pain in particular are phenomena that remain more in the realm of mystery than in clear understanding. The medical acupuncture

view of these phenomena closely parallels many aspects of the most instructive modern theories. The gate control theory holds that peripheral noxious signals are transmitted to the brain for conscious sensation via the spinal cord. These signals are modulated by other afferent inputs from the periphery and also by descending control from subcortical brain centers. In 2004, Melzack promulgated a revision to his original gate control theory which he terms the neuromatrix theory of pain. A revision of the original theory was prompted by clinical experience with amputees with phantom limb pain. These patients continue to experience identical patterns of arm pain, fatigue, itch, and movement in the absence of the affected limb. Out of these observations, a new theory is derived that focuses primarily on the brain. Melzack describes his neuromatrix theory subsequently. “The neuromatrix theory of pain proposes that pain is a multidimensional experience produced by characteristic “neurosignature” patterns of nerve impulses generated by a widely distributed neural network—the “body-self neuromatrix”—in the brain. These neurosignature patterns may be triggered by sensory inputs, but they may also be generated independently of them. Acute pains evoked by brief noxious inputs have been meticulously investigated by neuroscientists, and their sensory transmission mechanisms are generally well understood. In contrast, chronic pain syndromes, which are often characterized by severe pain associated with little or no discernible injury or pathology, remain a mystery. Furthermore, chronic psychological or physical stress is often associated with chronic pain, but the relationship is poorly understood. The  neuromatrix theory of pain provides a new conceptual framework to examine these problems. It proposes that the output patterns of the body-self neuromatrix activate perceptual, homeostatic, and behavioral programs after injury, pathology, or chronic stress. Pain, then, is produced by the output of a widely distributed neural network in the brain rather than directly by sensory input evoked by injury, inflammation, or other pathology. The neuromatrix, which is genetically determined and modified by sensory experience, is the primary mechanism that generates the neural pattern that produces pain. Its output pattern is determined by multiple influences, of which the somatic sensory input is only a part, that converge on the neuromatrix.”28 Melzack’s neuromatrix theory of pain shifts the focus away from the Cartesian concept of a one-to-one relationship between specific sensory experiences such as tissue damage or inflammation and the sensation of pain. This particularly applies to chronic pain states in which multiple factors such as psychological stress, physical injury, and cognitive states affect a genetically influenced and widely distributed neural network to produce multidimensional outputs such as the awareness and perception of pain as well as dysfunctional thoughts and action patterns. This theory, then, proposes a richly complex understanding of chronic pain that emphasizes the role of genetics, thoughts, emotions, physical sensations, stress pathophysiology, and the emerging field of psychoneuroimmunology. The medical acupuncture view of chronic pain has many parallels to Melzack’s neuromatrix theory, both in its understanding of the sources of chronic pain and in its treatment. Figure 17-1 illustrates the sensory inputs that influence the genetically determined neuromatrix: cognitive, sensory, and emotional. Medical acupuncture targets all of these inputs, the neuromatrix itself, and also the output programs that are often dysfunctional. Classical acupuncture often focuses on psychoemotional disturbances, whereas modern neuroanatomic acupuncture aims at

Medical Acupuncture  143 INPUTS TO BODY-SELF NEUROMATRIX FROM: COGNITIVE-RELATED BRAIN AREAS Memories of past experience, attention, meaning, anxiety SENSORY SIGNALING SYSTEMS Cutaneous, visceral, musculoskeletal inputs

BODY-SELF NEUROMATRIX C S A

EMOTION-RELATED BRAIN AREAS Limbic system and associated homeostatic/stress mechanisms

TIME

OUTPUTS TO BRAIN AREAS THAT PRODUCE: PAIN PERCEPTION Sensory, affective, and cognitive dimensions ACTION PROGRAMS Involuntary and voluntary action patterns STRESS-REGULATION PROGRAMS Cortisol, norepinephrine, and endorphin levels Immune system activity

TIME

Figure 17-1  Factors that contribute to the patterns of activity generated by the body-self neuromatrix, which is composed of sensory (S), affective (A), and cognitive (C) neuromodules. The output patterns from the neuromatrix produce the multiple dimensions of pain experience, as well as concurrent homeostatic and behavioral responses. (Adapted from Melzack R: Evolution of the neuromatrix theory of pain. The Prithvi Raj lecture: Presented at the Third World Congress of World Institute of Pain, Barcelona 2004. Pain Pract 5:85-94, 2005.)

treating musculoskeletal sources of dysfunctional inputs to the neuromatrix as well as spinal cord regions involved in spinal modulation. Scalp and auricular acupuncture are directed at affecting the neuromatrix itself. Acupuncture has also been shown to influence the stress regulation output program of the neuromatrix.22,29 While Melzack emphasizes the genetic contribution to the neuromatrix, classical acupuncture always strives to understand and treat the constitution of an individual, which can be understood as the genetically determined phenotype of an individual. The conventional biomedical approach to pain focuses evaluation and management strategies solely on the musculoskeletal sensory inputs to the neuromatrix, much in line with the Cartesian understanding of pain processing. And, within this subset of sensory inputs, the focus is even more narrowly put on joint, nerve, and tendon generators of afferent activity. The medical acupuncture approach to pain not only recognizes the value of treating all three groups of inputs to the neuromatrix (see Fig 17-1), but also focuses on an expanded set of tissues in the periphery capable of stimulating the neuromatrix. As such, medical acupuncture not only evaluates and treats dysfunctional joints, nerves, and tendons, but also muscle, ligaments, and fascia. Furthermore, medical acupuncture directs therapy at the neuromatrix itself and the stress response output program of the neuromatrix. This ability to comprehensively intervene at all points in ­Melzack’s neuromatrix theory for pain experience (sensory inputs, neuromatrix itself, and subsequent outputs) defines medical acupuncture as a uniquely robust therapeutic tool for the treatment of pain problems.

Mechanisms Twentieth Century Mechanisms Since its introduction to the American scientific community in the 1970s, acupuncture has often been perceived as a therapeutic modality whose mechanism is mysterious and unknown at best, and inert in terms of modern physiology at worst. Researchers who sought to prove the latter hypothesis as well as those who were curious about discovering possible physiologic mechanisms produced a prolific body of basic science data in the 1970s and 1980s. This research led to

the endorphin and monoamine hypothesis of acupuncture analgesia which has since been supported by an enormous collection of animal and human studies. Bruce Pomeranz, PhD, was one of the most prominent researchers in this area. He, indeed, set out to prove that acupuncture had no measurable physiologic effects. After publishing 66 papers investigating the mechanism of acupuncture analgesia, his conclusion was that the evidence supporting the endorphin hypothesis for acupuncture analgesia was stronger than that for almost any other therapeutic agent used in conventional medicine (Fig. 17-2). An acupuncture needle entering the skin and muscle in the arms or legs will activate unmyelinated C-fibers and small diameter myelinated A-delta fibers in the periphery that synapse onto cells of the anterolateral tract in the dorsal horn of the spinal cord. These cells give rise to two sets of projections. One set travels rostrally to eventually synapse on the midbrain, pituitary, and hypothalamus. The other set synapses on inhibitory interneurons in the spinal cord where dynorphin and enkephalin are released presynaptically to block ascending neurotransmission of painful signals along the spinothalamic tract. Meanwhile, the rostrally projecting cells of the anterolateral tract will stimulate cells in the periaqueductal gray causing the release of enkephalin, which will disinhibit cells of the raphe nucleus. The raphe nucleus is part of an endogenous descending analgesic pathway. Disinhibition of these cells activates this descending analgesic pathway, which causes the release of monoamines such as serotonin onto cells of the spinothalamic tract in the spinal cord that carry painful stimuli to the brain. Serotonin postsynaptically inhibits these cells, thereby dampening down the neurotransmission of painful signals from the periphery to the brain along the spinothalamic tract. Thus, the original acupuncture stimulus activates multiple neurochemical pathways in the brain and spinal cord and decreases the neuronal transmission of painful stimuli from the periphery to the brain.30 The ascending anterolateral tract neurons also stimulate the pituitary to release ACTH and β-endorphin into the bloodstream.30 Twenty-First Century Mechanisms Whereas 20th century research of the mechanism of acupuncture paralleled the discovery of the endorphin receptors and the gate control theory of pain, 21st century research is focusing on the brain, neuroimmunology, and connective tissue.

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STT 2

Painful stimulus

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E

M

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Mid brain

7 M

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Thalamus

Cortex

Pituitary hypothal

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14

Skin 9

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E E

E Muscle

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Acu needle

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5 Spinal cord Figure 17-2  Model developed from research by Dr. Pomeranz. (Adapted from Stux G, Pomeranz B (eds): Basics of Acupuncture: Berlin, 2005, Springer p27.

The research of Helene Langevin, MD focuses on the role of connective tissue as a dynamic whole body communication matrix and offers a fascinating model for the mechanism of acupuncture’s affect on the body. Loose connective tissue forms an anatomic network throughout the entire body. Most medical doctors spend little time thinking about fascia and connective tissue, and when they do, they think of it as purely structural in nature. In reality, fascia and connective tissue are intimately involved in complex regulatory mechanisms in the body such as ligandreceptor binding and gene transcription. Mechanotransduction is the biophysical process that is at the center of this research and forms the link between structure and function. Mechanotransduction is the process by which cells sense mechanical forces and transduce them into changes in intracellular biochemistry and gene expression. What is Fascia? Fascia is loose connective tissue that surrounds and interpenetrates all components of the human body including muscles, nerves, blood vessels, and organs. It provides structural integrity, serves as a matrix for intercellular communication, and is involved in biochemical and bioelectric signaling. The structural integrity of the soft tissue of the body is composed of a complex network of fascia and loose connective tissue on the macroscopic level and an equally complex microscopic network. The microscopic network is composed of an extracellular matrix of collagen and fibroblasts and an intracellular cytoskeleton of microfilaments, intermediate filaments, and microtubules. How Does Acupuncture Interact with Fascia and Loose ­Connective Tissue? The research of Langevin and colleagues has demonstrated that the twirling of the acupuncture needle that is typical in clinical practice creates mechanical changes in the collagen and fibroblast network of the extracellular matrix. In fact, her work using histologic sections and specialized ultrasonography has shown that

the manipulation of the acupuncture needle produces characteristic changes in the surrounding loose connective tissue such as the wrapping of collagen fibers. She has demonstrated that these mechanical changes in the connective tissue are accompanied by active cellular changes such as lamellapodia formation and fibroblast spreading. Although not yet conclusive, this research supports the hypothesis that acupuncture needling activates diverse biological processes such as gene transcription, protein synthesis, and neuromodulation through the mechanism of mechanotransduction (Fig. 17-3). These biochemical phenomena may underlie many of the unknown mechanisms of the therapeutic effects of acupuncture.31-34 Biochemical Milieu of Trigger Points Although the subject is not as novel as the work of Langevin and colleagues, the research of Jay Shah, MD is equally fascinating and instructive. Clinicians have long relied on the pioneering work of Janet Travell, MD in treating myofascial pain. Trigger point needling with and without local anesthetic is used by medical acupuncturists to treat many types of myofascial pain. However, until recently, convincing basic science research characterizing the qualities of trigger points has been lacking. In the January 2008 publication of The Archives of Physical Medicine and Rehabilitation, Dr. Shah describes an innovative technology that allows the real time biochemical assay of the trigger point milieu. A 30-gauge microdialysis needle is used to noninvasively sample 11 histochemicals in clinically identified trigger points. This study confirms that biochemicals associated with pain and inflammation (protons, substance P, TNF-α, bradykinin, and many others) are present in higher concentration in active trigger points than in latent trigger points and control muscle points. Furthermore, after needling the trigger points, concentrations of substance P, and CGRP are shown to decline. Though requiring additional study, this work offers a convincing basic science explication for the mechanisms underlying the dry needling of trigger points that is an integral part of medical acupuncture.35,36

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Rotation

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Collagen

Focal adhesion F-actin

Mechanoreceptor/ nociceptor

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SENSORY AFFERENTS

Winding

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FIBROBLASTS Mechanotransduction

Mechanotransduction

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Actin polym.

Cell contraction ERK phosphorylation

Mechanotransduction

Actin polymerization

Cell contraction

ERK phosphorylation

Cell contraction

ERK phosphorylation

Gene expression, protein synthesis, and secretion

Extracellular milieu modification

Neuromodulation

Figure 17-3  Hypothesis summary. Proposed mechanical signal transduction and downstream effects of acupuncture needle manipulation at gross and microscopic levels. Shaded areas represent deep connective tissue planes of the upper arm. The acupuncture needle is inserted on the lateral border of the biceps. Arrows represent pulling of connective tissue and matrix deformation during acupuncture needle manipulation. The “lung” acupuncture meridian is located along the lateral border of the biceps and may coincide with some of the outlined connective tissue planes. (Adapted from Langevin HM, Churchill DL, Cipolla MJ: Mechanical signaling through connective tissue: A mechanism for the therapeutic effect of acupuncture. FASEB J 15: 2275-2282, 2001.)

Brain Imaging Extensive animal and human data indicate that many of the beneficial effects of acupuncture are mediated through the central nervous system. However, whereas mechanisms such as central modulation of endorphins and monoamines and the recruitment of the midbrain descending analgesia system are well characterized, much is not known about how acupuncture interacts with the CNS. In the last decade, interest has accelerated in the use of functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) imaging to further understand the effects of acupuncture on the brain.

Acupuncture Effects on the Brain Nonpainful stimulation of peripheral nerves using transcutaneous electrical stimulation causes an increase in activation of the somatosensory, motor, premotor, posterior parietal, and cingulate cortices, as well as the thalamus and cerebellum as measured by fMRI.37,38 Painful stimuli produce activation in multiple regions of the brain including the primary and secondary somatosensory cortices, the insular cortex, the anterior cingulate cortex, the thalamus, and the prefrontal cortex.39 Reproducible data show that acupuncture modulates an extensive network of cortical, subcortical, and brainstem regions

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Digit 2

CTS: Baseline CS

L (contra)

CTS: Postacupuncture

R (ipsi)

PreCG Digit 3

SI

Digit 5

SII

Figure 17-4  Group maps of CTS patients at baseline and postacupuncture for D2, D3, and D5 nonnoxious electrostimulation. Activation (color-coded P-value) was overlaid onto group-averaged inflated brains with gray-scale defined curvature (sulci dark, gyri light). Both right (ipsilateral) and left (contralateral) hemispheres are shown. Hyperactivity in contralateral sensorimotor cortex seen for median nerve innervated D3 diminished after acupuncture treatment. Differences for D2 and ulnar nerve innervated D5 were less profound. Contra, Contralateral; CS, Central sulcus; CTS, CT scan; ipsi, Ipsilateral; SI, SII. (From Napadow V, Liu J, Li M, et al: Somatosensory cortical plasticity in carpal tunnel syndrome treated by acupuncture. Human Brain Mapping 28:159-171, 2007.)

in the brain.40 Numerous fMRI studies have demonstrated that acupuncture elicits a response in multiple cortical regions including the primary and secondary somatosensory cortices, the insular cortex, and the prefrontal cortex when compared to a variety of needle and nonneedle controls.40 A robust limbic network, including the hippocampus, amygdala, hypothalamus, and anterior cingulate cortex is also modulated.41 Brainstem structures involved in endogenous descending analgesia such as the periaqueductal gray are recruited by acupuncture therapy.42 Whereas nonacupuncture transcutaneous stimulation of peripheral nerves and painful peripheral stimuli generally produce an increase in signaling in the brain’s pain matrix, acupuncture therapy produces a modulation or a decrease in signaling intensity in the same regions of the brain.22 Interestingly, acupuncture stimulates widespread deactivation of brain regions involved in the affective and cognitive aspects of pain, and also is able to influence the brain structures that control the physiologic stress response. The amygdala translates somatosensory stimuli into affective states. The amygdala exhibits patterns of sensitization and hyperactivation in response to chronic pain states.43 Acupuncture therapy elicits deactivation of the amygdala in healthy controls and in patients with chronic pain. Additional limbic structures involved in consolidation of somatosensory memory and the interface of cognitive and emotional mentation are also affected by acupuncture.22,29 The hypothalamus receives and integrates diverse information about the internal and external environment and produces a coordinated output program. A major aspect of hypothalamic output is orchestration of the body’s response to physiologic and psychological stress through the hypothalamicpituitary-adrenal axis. The classical descriptions of acupuncture encouraging a return to homeostasis in the body are interesting in light of recent fMRI research demonstrating modulation of the hypothalamus in pain states.22,29,41

Napadow and colleagues have also explored the effects of acupuncture on the dysfunctional neuroplasticity that develops in chronic pain patients. This dysfunctional central neuroplasticity may be part of the basis for their persistent pain, and its correction may underlie some of the therapeutic effects of acupuncture in chronic pain states.29,44,45 A fascinating set of studies by this group has evaluated the brain effects of acupuncture on carpal tunnel syndrome (CTS) patients versus healthy controls. For the patients with CTS, the region of the sensorimotor cortex subserving the first three digits of the affected hand demonstrated hyperexcitability to nonnoxious stimuli when compared to healthy controls. After 13 acupuncture treatments performed over 5 weeks, the dysfunctional cortical hyperexcitability seen in the carpal tunnel patients diminished significantly. Healthy controls did not exhibit a similar rearrangement in cortical activity. These studies are an excellent example of the beneficial neuroplasticity that can be induced by acupuncture therapy.22,44,45 Figure 17-4 illustrates group-averaged difference mapping of the contralateral sensorimotor cortex for CTS patients before and after acupuncture. Hyperactivity to nonnoxious stimuli in the contralateral sensorimotor cortex was exhibited in the median nerve innervated third digit at baseline. This hyperactivity in the third digit diminished after acupuncture treatment. Activation of Neuronal Networks Central nervous system disorders such as Parkinson disease, chronic pain, and depression are thought to involve the disruption of key neuronal networks. Faingold hypothesizes that electrical stimulation therapies such as deep brain stimulation, vagus nerve stimulation, electroconvulsive therapy, and acupuncture exert their therapeutic effects by recruiting dormant neuronal networks that compete with and override the pathologic networks mediating

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disease. It is suggested that the overall manifestation of symptoms by the individual is determined by which neuronal network (pathologic or therapeutic) prevails and achieves control of the affected brain function. Thus, Faingold postulates that the mechanism of electrical stimulation therapies such as acupuncture involves the stimulation of potentially therapeutic dormant neuronal networks that subsequently manifest as elimination or diminution in symptoms.46

Does Needling of Acupuncture Points Produce Different Brain Activation Patterns than Needling of Nonclassically Defined Body Locations? Why is this an interesting question? On the one hand, practitioners of classical acupuncture are eager to demonstrate that the needling of classically defined acupuncture points produces significantly different effects from the needling of nonclassically defined locations. On the other hand, several large and well done clinical studies of acupuncture have yielded similar clinical benefits for patients treated with classical acupuncture and minimal acupuncture, which is variably defined as superficial needling at classical acupuncture points and needling at nonclassical locations, when compared to patients receiving standard conventional treatments.47-49 Other large clinical studies show a significant clinical difference in the benefit achieved with classical versus nonclassical needling. From the clinical standpoint, it is clear that most needling interventions (classical acupuncture and minimal acupuncture) have a beneficial effect. Point selection may be less important in determining clinical efficacy. Exploring the differential neurobiologic effects of needling classical versus nonclassical locations will aid in the understanding of this phenomenon observed in clinical trials. Data from fMRI Studies Wu and colleagues observed that electroacupuncture at a nonacupuncture point (sham acupuncture) produced some of the same cortical changes as electroacupuncture at a classical acupuncture point (real acupuncture). Both sham and real acupuncture produced similar effects in the caudal segment of the anterior cingulate cortex, insula, secondary somatosensory cortex, thalamus, and cerebellum. However, real acupuncture produced additional effects in the limbic system not observed with sham acupuncture. Specifically, difference mapping demonstrated activation of the hypothalamus and deactivation of the anterior cingulate cortex with real acupuncture versus sham acupuncture.50 Acupoint Specific Brain Activation There are data to support the notion that acupuncture points exert a specific pattern of stimulation of the brain corresponding to the classical descriptions of the points.51 These results, however, have not been consistently reproduced.

Optimal Acupuncture Therapy for Pain The evaluation of the painful condition follows the framework of a general medical evaluation. A detailed history is obtained from the patient with care to elicit clues to the neuromusculoskeletal source of the pain, psychoemotional interplay, components of maldynia such as dysfunctional thoughts, beliefs, and actions, as well as pertinent aspects of social relationships, and the patient’s underlying constitution. A detailed and focused physical examination is performed with particular attention to finding a neuromusculoskeletal

source as well as any contributing underlying or secondary factors. This is an area that may receive greater attention than in modern pain medicine. For example, a patient with postsurgical pain may receive a diagnosis of adhesions producing visceral pain or neuropathic denervation pain from a pain physician with all therapies aimed at this particular diagnosis. The physician acupuncturist will not only identify and address the underlying denervation pain, but will also explore the possibility of myofascial dysfunction that exacerbates the neuropathic pain. By treating the secondary myofascial component, the neuropathic aspect may become more amenable to treatment. Optimal acupuncture therapy for pain problems involves matching the most appropriate neuroanatomical acupuncture techniques with the patient’s neuromusculoskeletal diagnosis. This neuroanatomic acupuncture input is then reinforced by microsystem therapy and classical acupuncture therapy. Determining a precise NMS understanding of the presenting pain problem, then, is central to the medical acupuncture approach to pain. The NMS diagnosis will attempt to identify primary, secondary, and tertiary dysfunction at various levels in the physical organism. Neuromusculoskeletal Diagnosis A precise NMS diagnosis identifies specific areas of dysfunction in the structure of the physical body and at various points in the nervous system. Physical examination maneuvers and knowledge of the functional anatomy are combined to locate primary, secondary, and tertiary problems in the following zones: skin and subcutaneous tissues, superficial fascia, surface and deep muscles, myotendinous junctions, tendons, bursae, joints, ligaments, and bone. Similarly, subjective descriptions of the pain by the patient, physical examination maneuvers, and knowledge of the neurophysiology of pain are used to determine areas of dysfunction in the nervous system: Peripheral nerve, neuromuscular, spinal cord, and brain. When the structural and neurologic aspects of the pain problems have been clearly identified, the physician acupuncturist will select from a wide array of needling techniques to address the lesions. These therapeutic inputs are designed to alter the peripheral nociceptive inputs while also addressing the abnormal neuronal processing of pain signals that characterizes many chronic pain problems. For example, consider a patient with painful peripheral diabetic neuropathy. An initial peripheral input will supply electrical stimulation to acupuncture needles inserted adjacent to the interdigital nerves of the hands or feet. A variety of electrical frequencies can be applied during the same treatment or sequentially at successive treatments. This basic peripheral input can be augmented by vibratory stimulation of the richly innervated interosseus membrane of the forearm or leg with the intent of disrupting dysfunctional dysregulation of the autonomic nervous system. The  central pathologic changes that often occur in many chronic pain states can be addressed with acupuncture inputs that influence the spinal nerves corresponding to the dermatome, myotome, sclerotome, and splanchnotome of the pain problem. Neuroanatomic acupuncture inputs are designed to address various aspects of the neuromusculoskeletal system and are ideally suited for addressing the interrelated NMS matrix of the body. The physician acupuncturist seeks to identify and correct the dysfunctions of the NMS matrix that occur in pain states. One important aspect of systems of classification, such as medical diagnosis, is identifying clinical entities that are likely to

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respond to particular treatments. With this in mind, the physician acupuncturist explores the NMS matrix of the pain patient for clinical syndromes that respond to NMS acupuncture inputs. For example, the physician acupuncturist does not rely solely on pathodiagnostic classifications such as herniated lumbar disc or lateral epicondylitis. Rather, these diagnoses are used as starting points and additional contributing factors are sought. Commonly, muscular trigger points and tightness of the superficial fascia will complicate and exacerbate pain considered to be neuropathic in origin. Similarly, abnormal regional and spinal segmental neuronal processing will often accompany muscular, ligamentous, and tendinopathic pain. Recognizing these interrelated dysfunctions of pain problems is particularly important and germane because acupuncture is well suited to address muscular, fascial, neuronal, tendinous, ligamentous, and visceral dysfunctions.24,31,35,52 Pain is a Mind Body Problem and Medical Acupuncture is a Mind Body Treatment Pain is a unique medical problem that cuts across virtually all areas of medicine. At its core it epitomizes all of the subtleties and complexities of mind-body holism. It is now clear that any model seeking to explain the experience and pathogenesis of pain is incomplete if it omits the impact of our thoughts and feelings, actions, social relationships, or biomedical makeup. The arena of pain medicine matches these multifaceted aspects of pain with the multidisciplinary pain clinic that houses—under one roof—biomedical pain specialists emphasizing interventional and pharmaceutical approaches, psychologists addressing the psychoemotional component of pain, physical therapists with expertise in reconditioning and manual techniques, and a hodge-podge of complementary techniques primarily based on market demand. Unfortunately, the economic situation of modern medicine in the United States at the beginning of the 21st century fosters fragmented, intervention-based medical care even within multidisciplinary pain clinics. In fact, economic necessity is now the organizing principle of many multidisciplinary pain clinics compared to the original founding goal of offering truly holistic pain medicine based on the biopsychosocial model. Although many interventional approaches have little evidence for efficacy,53-55 they are reimbursed by third party payers at high rates and therefore generate the majority of revenue at multidisciplinary pain clinics. Because of this, these invasive therapies are often used more frequently than less expensive, conservative therapies based on the biopsychosocial model of pain that are supported by stronger evidence.56 Because medical acupuncture provides a framework for evaluating and treating physical, emotional, and psychological aspects of a patient, it can serve as a model for the multifaceted management of pain problems. Ideally, the medical acupuncture management of complex pain problems takes place within an integrated medical team. The integration of medical acupuncture within the greater system of pain medicine is discussed subsequently. As a therapeutic input that provides an orchestrated therapy directed at a patient’s psychoemotional state and neuromusculoskeletal dysfunctions, medical acupuncture is uniquely suited to address many of the complexities inherent in the pain patient. As is well known to pain medicine physicians, many patients with subacute or longstanding pain problems exhibit dysfunctional sleep, relationships, thought patterns, emotions, and behaviors. As discussed earlier, optimal acupuncture for pain seeks to address, and is capable of affecting, all of these elements.

Safety Acupuncture performed by a medically trained practitioner is a relatively safe and forgiving procedure. It is difficult to introduce new or persistent problems with acupuncture therapy. Acupuncture treatments commonly induce a state of relaxation especially when electrical stimulation is used. Sometimes this state can evolve into or be perceived as fatigue or dysphoria, particularly by those accustomed to the physiologic milieu of a tonically activated stress system. The principal serious adverse effects caused by acupuncture are vasovagal syncope, puncture of an organ, infection, and a retained needle. These risks can be minimized by using single-use or sterilized needles, obtaining appropriate clinical training, understanding surface and internal anatomy, and exercising sound clinical judgment. A systematic review of nine surveys of the safety of acupuncture involving more the 250,000 treatments found that feelings of faintness and syncope occurred in less than 0.3% of treatments. Feelings of relaxation were common and occurred in almost all patients (86%).57 Of the serious adverse effects, pneumothorax is one of the most common. The large Acupuncture Safety and Health Economic Studies (ASH) in Germany involved more than 1.6 ­million ­acupuncture sessions and reported two pneumothoraces for an occurrence rate per session of less than 0.0001%.58 This same research initiative reported local infection in 0.3% of patients.58 Cost Effectiveness of Acupuncture All healthcare delivery systems must consider the relative economic costs and comparative benefits of medical treatment options. In countries where healthcare is administered largely according to payment by a national insurance system, cost-effectiveness metrics have been developed to facilitate cost-benefit analyses and ultimately aid in deciding what medical treatments will be available. In the United Kingdom a value of less than 30,000 pounds per quality adjusted life year (QALY) has been set by the National Institute for Health and Clinical Excellence (NICE) as representing a cost effective therapy. Cost-effectiveness research for acupuncture has been conducted with data from the national health insurance systems of Germany and England. Using acupuncture for the treatment of headache, chronic neck pain, low back pain, and osteoarthritis of the knee and hip has been shown to be cost effective using accepted international thresholds. In the largest clinical investigation of acupuncture to date, ­German researchers evaluated the cost effectiveness of acupuncture for the treatment of headache, chronic neck pain, low back pain, and osteoarthritis of the knee and hip in the Acupuncture in Routine Care Studies (ARC).47 ARC included nearly 8500 patients for economic analysis and found acupuncture to be effective for all diagnoses studied with an average increase in expenditure of 319  euros per treatment course.47,58 The cost effectiveness was found to be between 10,526 euros per QALY for low back pain and 17,854 euros per QALY for knee and hip osteoarthritis. Thus, acupuncture for all diagnoses was found to be well within accepted standards for cost effectiveness. British researchers evaluated the cost effectiveness of acupuncture for the treatment of chronic headache and found that acupuncture improved quality of life for a relatively small incremental cost. They estimated that acupuncture treatment resulted in a cost of 9180 pounds per QALY which compares favorably to medication treatment of migraine headaches. Substituting oral sumatriptan for oral caffeine plus ergotamine results in a cost of 16,000 pounds per

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QALY.59,60 Other studies have found acupuncture to be cost effective for chronic neck pain with a cost of 12,469 euros per QALY61 and low back pain with a cost of 4241 pounds per QALY.62

Clinical Research Virtually all studies of acupuncture for the treatment of pain show substantial efficacy when compared to control groups that consist of waiting list populations receiving standard conventional therapy. Studies comparing true acupuncture with nonpenetrating sham control groups are more mixed, but the majority demonstrate incremental benefit of true acupuncture over nonpenetrating sham groups. Significant benefit of needling traditional acupuncture points over needling nontraditional locations has also been repeatedly demonstrated, however, the effect size is considerably reduced, and the results are less consistent. This would be expected from our knowledge of the physiologically active effects of needle penetration. Acupuncture points are not magical nor do they possess inexplicably different properties compared to other locations in the body. Classical acupuncture points can be viewed as physiologic hot spots in the body that have been discovered through several millennia of empirical investigation. They often correspond to trigger points, connective tissue cleavage planes, accessibility of peripheral nerves, and regions of densely concentrated neurovascular bundles. Many other locations on the body have similar neuroanatomic characteristics, but are not described as classical acupuncture points. These locations will likely have many of the same physiologic and clinical effects as classically defined acupuncture points. Acupuncture points and nonacupuncture points are often discussed as black and white distinctions. The preceding brief description of various systems of acupuncture underscores the diverse conceptions of acupuncture points and acupuncture needling techniques. When one considers the vast multitude of classically defined “extra” points, the superficial needling technique used in Japanese acupuncture, and the shifting point locations described by Ryodoraku acupuncture, the near impossible task of defining “nonacupuncture” points even from the classical perspective becomes evident. Challenges of Studying Acupuncture Since the 1950s the randomized, double blind, placebo controlled trial (RDBPCT) has become the standard methodology for evaluating the effectiveness of pharmaceutical therapies. Although going to great lengths to exclude bias, this methodology also has its limitations. Perhaps the most vexing problem of the RDBPCT is the discordance between what is studied (homogeneous patients without comorbid conditions) and real life (complex patients with multiple medical problems).63-65 Furthermore, the RDBPCT may not be the best method to evaluate complex medical interventions such as surgery, physical therapy, psychotherapy, and acupuncture. In contrast to pharmaceutical therapy, the substance of these interventions cannot be divorced from the mode of delivery. Because of this, controls that allow clear isolation of the “specific” effects of the intervention from the “nonspecific” effects of the delivery mode are virtually impossible to devise. For example, it is impossible to magically remove a gallbladder without going through the lengthy and ritualized preoperative intake, intraoperative anesthesia, and postoperative recovery process. In the case of acupuncture, we know that sham acupuncture is a myth. Sham acupuncture or minimal acupuncture is generally

defined as the insertion of needles at so called “nonacupuncture” points or at shallow depths over classically defined acupuncture points, and is considered to be physiologically and clinically inert. Sham needling at “nonacupuncture” locations is problematic for several reasons. From classical as well as modern reasoning, it is virtually impossible to find a location on the body that will not produce a physiologic action in response to acupuncture needling. There are roughly 360 body locations called “meridian points” that are avoided to find “nonacupuncture” points. Interestingly, there are several thousand “extra-meridian” acupuncture points and a multitude of points that are located based on the specific manifestation of symptoms of each person, making the selection of “nonacupuncture” points challenging at best from the classical perspective. Likewise, modern fMRI research has demonstrated that while needle stimulation at acupuncture points produces more robust brain modulation than needle stimulation at “nonacupuncture” points, nonacupuncture points are physiologically active.50 For the goal of separating the needling effects of acupuncture from the effects of the ritual of delivering acupuncture, sham acupuncture devices such as the Park Sham Device may represent an improvement over shallow needle insertion at acupuncture points or needle insertion at “nonacupuncture” points. The Park Sham Device uses a retractable blunt-tipped needle that does not penetrate the skin. However, it is important to note that although a needle does not pierce the skin when using the Park Sham Device, skin contact is made. This skin contact will likely produce similar effects as the Japanese acupuncture procedure known as teishin, in which a blunt-tipped probe is used to apply light pressure over acupuncture points. A more useful methodology for studying complex interventions such as acupuncture may be the pragmatic randomized controlled trial (PRCT).66 The PRCT evaluates actual questions facing the practicing clinician. For example, in a patient with refractory depression managed by the primary care physician, does referral for collaboration with a psychiatrist result in improved patient outcomes?67 Or will a patient with chronic low back pain receiving conventional management from the primary care provider derive additional incremental benefit from a referral to medical acupuncture? Key features of the PRCT are minimizing exclusion criteria in an attempt to match the study population more closely with the heterogeneous types of patients encountered in clinical medicine as well as using pragmatically selected control groups such as a “treatment as usual group”.66 Although marked improvements have been attributed to placebo interventions such as the “sugar pill,” the actual improvement beyond treatment as usual groups may be minimal or nil. A 2004 Cochrane review of placebo interventions for all clinical conditions concluded “There was no evidence that placebo interventions in general have clinically important effects. A possible small effect on continuous patient-reported outcomes, especially pain, could not be clearly distinguished from bias,” and further “It has been widely believed that placebo treatments are associated with substantial effects on a wide range of health problems. However, this belief is not based on evidence from randomized trials that use a placebo treatment for one group of people, while another group receives no treatment. The effect of placebo treatments was studied by reviewing more than 150 such trials covering many types of health care problems. Placebo treatments caused no major health benefits, although they possibly had a small effect on outcomes reported by patients, for example, pain.”68

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When evaluating the effectiveness of a therapeutic intervention, it is imperative to use control groups to account for spontaneous improvement in symptoms and the fluctuation in symptoms that is inherent to the natural course of a disease process. When the evaluated therapy is simple, such as pharmacotherapy, and the substance of the intervention can easily be separated from the process of the intervention, using a placebo pill may be useful to account for additional bias such as expectancy. However, when evaluating the relative clinical effectiveness of complex interventions such as psychotherapy, surgery, and acupuncture where the substance and process of the therapy are inextricable, use of control groups that consist of treatment as usual or an alternate therapy [acupuncture versus physical therapy or percutaneous coronary intervention (PCI) versus coronary artery bypass grafting (CABG)]69 may provide more clinically relevant information. Spine Pain A Cochrane review of acupuncture and dry needling for low back pain including 35 RCTs through 2003 concluded that acupuncture is effective for pain relief and functional improvement of chronic low back pain when compared to either usual treatment or sham acupuncture. Improvement was noted immediately after a course of acupuncture and for up to 3 months after the cessation of treatments. Acupuncture was also found to offer incremental benefit in pain reduction when added to standard treatments for chronic low back pain.70 Three large German RCTs published after the Cochrane review demonstrated a substantial reduction in low back pain for acupuncture relative to standard conventional treatments for periods extending to 6 and 12 months. Haake and colleagues randomized 1162 patients with back pain to acupuncture according to classical concepts, superficial acupuncture needling at nonacupuncture points, or usual care consisting of drugs, physical therapy, and exercise. The primary outcome was improvement in pain or function at 6 months. Both needling groups were almost twice as likely to improve when compared to usual conventional care. There was little difference between the two acupuncture groups suggesting that point selection may be less important than proposed by classical acupuncturists.49 Brinkhaus and coworkers found similar results in a rigorously designed RCT with improvement maintained through 12 months.71 Witt and associates included 11,630 patients in a study evaluating clinical and economic effectiveness of acupuncture for low back pain. Of 3093 patients who consented to randomization, 1549 patients were allocated to receive immediate acupuncture and 1544 patients were allocated to a waiting list control group that would receive acupuncture 3 months later. The  remaining 8537 who did not agree to randomization generally had more severe baseline symptoms and were included in a nonrandomized cohort. In the randomized arm, acupuncture was found to be effective at reducing pain and function when compared to routine care with an absolute risk reduction of 25.8%, yielding a number needed to treat of four. Interestingly, the nonrandomized acupuncture cohort with more severe baseline symptoms experienced improvement in pain and function similar to the randomized group receiving acupuncture.48 Fewer studies have been conducted for neck pain, however a high-quality meta-analysis has been performed. A Cochrane review of acupuncture for neck disorders including 10 RCTs through 2006 found moderate evidence that acupuncture was more effective at relieving pain than sham treatments for both mechanical neck pain and neck pain with radicular symptoms for up to 3 months.72

Headache In 2009, The Cochrane Collaboration published two meta-analyses evaluating the use of acupuncture for prophylaxis of migraine and tension-type headaches. Their review of acupuncture for migraine prophylaxis included 22 RCTs through April 2008. The authors concluded that “…Available studies suggest that acupuncture is at least as effective as, or possibly more effective than, prophylactic drug treatment, and has fewer adverse effects. Acupuncture should be considered a treatment option for patients willing to undergo this treatment.” They also state “…There is no evidence for an effect of ‘true’ acupuncture over sham interventions, though this is difficult to interpret, as exact point location could be of limited importance.”73 The same authors reviewed the effects of acupuncture for tension-type headache and included 11 RCTs through January 2008. They concluded that “…acupuncture could be a valuable nonpharmacological tool in patients with frequent episodic or chronic tension-type headaches…”. They report that two large RCTs compared acupuncture to usual care and found 47% of patients receiving acupuncture experienced a reduction in headache frequency by at least 50% compared to 16% of the patients in the control group. They also describe six RCTs that compared ‘true’ acupuncture to ‘fake’ acupuncture in which needles are either inserted at ‘incorrect’ points or did not penetrate the skin. The pooled analysis of these RCTs revealed a small, but statistically significant improvement of the patients receiving ‘true’ acupuncture versus ‘fake’ acupuncture. That is, 50% of patients receiving true acupuncture reported a reduction of at least 50% in headache frequency versus 41% of patients receiving ‘fake’ acupuncture.74 A 2007 German review concluded that a 6-week course of ­acupuncture treatments is equivalent to a 6-month course of prophylactic drug treatment. This review also suggested that traditional concepts of needle location and stimulation are not as important as had been thought, and recommended “that acupuncture should be integrated into existing migraine therapy protocols.”75 Several RCTs have also evaluated the use of acupuncture for acute migraine headache. A recent RCT published in Headache in 2009 randomized 175 patients to receive true acupuncture or one of two sham acupuncture groups who received needling at various nonacupuncture points. The true acupuncture group experienced a greater decease in pain versus the sham acupuncture groups at 2 and 4 hours after treatment. In addition, 40.7% of those receiving true acupuncture experienced a complete resolution of pain within 24 hours versus 16.7% and 16.4% in the two sham acupuncture groups.76 Melchart and colleagues randomized 179 migraine patients to receive acupuncture, subcutaneous sumatriptan, or a placebo injection at the first sign of a migraine headache. Acupuncture and sumatriptan were equally effective in preventing a full migraine attack. Acupuncture resulted in a 21% absolute risk reduction and sumatriptan resulted in a 22% absolute risk reduction when compared to the placebo injection. If a full attack could not be prevented, sumatriptan was more effective than acupuncture in reducing pain. Side effects were more common in patients who received suma­ triptan (40%) than in acupuncture patients (23%) or patients who received the placebo injection (16%).77 Knee Pain White and colleagues published a 2007 meta-analysis in the journal Rheumatology which reviewed 13 RCTs investigating the effect of acupuncture on pain and function in patients with chronic knee

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pain. This review concluded that acupuncture improves pain and function in patients with chronic knee pain when compared to sham acupuncture and usual care.78 A second meta-analysis published by Manheimer in the Annals of Internal Medicine in 2007 included 11 RCTs and concluded that, when compared to waiting list controls, acupuncture results in clinically relevant benefits in patients with osteoarthritis of the knee. Short term benefits were also found in trials that used sham control groups, but these were deemed to be not clinically relevant.79 Two of the largest high-quality RCTs were conducted in Germany and published in 200520 and 2006.21 Both of these trials showed incremental benefit for acupuncture in patients with knee osteoarthritis when compared to conventional treatment. The trials yielded conflicting results regarding differences between classical acupuncture and minimal acupuncture. Shoulder Pain Fewer large, high-quality trials are available to evaluate the effectiveness of noninvasive therapies for chronic shoulder pain. Cochrane reviews for acupuncture, physical therapy, and corticosteroid injections have concluded that insufficient evidence exists to guide therapy for these interventions.80-82 Subsequent to the publication of the Cochrane meta-analysis for acupuncture, Guerra de Hoyos and coworkers published the largest RCT to date in 2004.83 This study randomized 130 patients with chronic shoulder pain to active acupuncture or nonpenetration control acupuncture and demonstrated an improvement in pain intensity and every secondary outcome measure 3 and 6 months after treatment. A 2005 RCT published in the journal Physical Therapy evaluated the effectiveness of ultrasound or acupuncture added to exercise therapy in 85  patients with impingement syndrome. This study included follow-up data for 12  months and concluded that the addition of acupuncture to home exercises was more effective than the addition of ultrasound.84 The largest high-quality RCT was published in the journal Rheumatology in 2008 and evaluated the effect of adding a single acupuncture point to physical therapy in 425 patients with shoulder pain. The acupuncture group experienced reduced pain as well as a reduction in analgesic medication consumption in comparison to the control group which received only physical therapy.85 Elbow Pain A 2004 meta-analysis published in the journal Rheumatology included 6 RCTs evaluating the effectiveness of acupuncture for lateral epicondylar pain. All six of the studies demonstrated that acupuncture was effective at relieving lateral epicondylar pain for up to 3 months after a course of treatments. Five of the six studies demonstrated superiority of acupuncture when compared to control treatments.86 A systematic review investigating the effectiveness of conservative therapies in the rehabilitation of lateral epicondylitis was published in the Journal of Hand Therapy in 2004 and came to similar conclusions.87 Hip Pain Few high-quality RCTs have been conducted to evaluate the effectiveness of acupuncture for hip pain. A small RCT published in the Clinical Journal of Pain in 2004 compared electroacupuncture to patient education in patients with osteoarthritis related hip pain. Electroacupuncture was significantly more effective at reducing pain and improving functional status and quality of life when compared to patient education at all three assessment periods: immediately after a course of treatment, as well as 3 and 6 months after a course of treatment.88

A much larger high-quality study was published by Witt and colleagues in Arthritis and Rheumatism in 2006 as part of the colossal German Acupuncture trials. In this study 712 patients with hip or knee osteoarthritis (45% had hip osteoarthritis) were randomized to receive acupuncture or standard medical therapy. In addition, a nonrandomized cohort of 2921 patients with identical baseline characteristics was included in the study. In the randomized group, patients receiving acupuncture experienced a marked clinical improvement compared to patients receiving standard medical therapy. These improvements were maintained up to 6 months after treatment. Interestingly, the outcomes for the large nonrandomized group receiving acupuncture were similar to those experienced by the group randomized to receive acupuncture.89 Fibromyalgia Evidence for the effectiveness of acupuncture for fibromyalgia is sparse and conflicting. A 2006 literature review included five RCTs, of which three demonstrated effectiveness of acupuncture versus sham treatment and two showed a lack of effectiveness. Because of the heterogeneity of the abstracted data, meta-analysis was not possible. Number of treatments did not seem to affect the likelihood of positive response. Interestingly, all of the RCTs that demonstrated effectiveness for the acupuncture group used electroacupuncture, whereas the two RCTs that failed to demonstrate effectiveness used manual stimulation only. This review concludes that acupuncture for the symptomatic treatment of fibromyalgia is not supported by unanimous results from RCTs.90 Temporomandibular Joint Pain High-quality research investigating the efficacy of acupuncture for temporomandibular joint related pain is limited. A literature review published in 2001 evaluated 14 studies. The three RCTs that met inclusion criteria evaluated acupuncture versus occlusal splints with two studies also including usual care control groups. All three RCTs that were included found acupuncture to be effective in a variety of metrics including the visual analog scale, mandibular function, and number of tender points on examination. The degree of effectiveness, however, was not quantified.91 A small RCT published in 2006 evaluated true acupuncture versus noninsertional sham acupuncture using a single needle on the face. Multiple endpoints were recorded and found to favor true acupuncture. The group receiving true acupuncture reported a 53% reduction in pain on the visual analog scale versus a 6% reduction reported by the sham group. Likewise, the true acupuncture group reported a 55% reduction in functional impairment versus a 6% reduction reported by the sham group.92 Postoperative Pain A systematic review of 15 RCTs evaluating acupuncture for postoperative pain was published in The British Journal of Anaesthesia in 2008. The data were analyzed for postoperative opioid consumption, postoperative pain intensity, and opioid-related side-effects. Acupuncture was found to have an opioid-sparing effect at 8 hours, 24 hours, and 72 hours corresponding to a respective 21%, 23%, and 29% reduction of morphine consumption, respectively. A moderate and statistically significant reduction in pain intensity was found at 8 and 72 hours in the acupuncture treatment groups. A statistically significant reduction in opioid-related adverse affects was also found. Treatment by acupuncture was associated with a 33%  ­reduction in the incidence of nausea, a 35% reduction in

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dizziness, a 22% reduction in sedation, a 25% reduction in pruritus, and a 71% reduction in urinary retention.93 Auricular acupuncture has also been studied in the postoperative period. Usichenko and associates studied 54 patients undergoing total hip arthroplasty and compared four acupuncture press tacks in the ear at acupuncture points versus nonacupuncture points. The group that received acupuncture at acupuncture points of the ear used 31% less opioid administered by a patient-controlled analgesia pump and had similar pain intensity scores measured by the visual analog scale.94 Taguchi and coworkers studied the effect of acupuncture on anesthetic requirement in healthy volunteers in a rigorous doubleblind experiment. This group found that healthy volunteers who received auricular acupuncture at four points required 8.5% less desflurane anesthesia to prevent movement in response to noxious stimuli when compared to healthy volunteers who did not receive auricular acupuncture.95 Miscellaneous Preliminary evidence from small but well done RCTs suggests that acupuncture is effective at relieving symptoms in patients with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). The most recent study recruited 63 patients who met the U.S National Institutes of Health (NIH) consensus criteria for CP/CPPS in a three arm RCT. The electroacupuncture group received acupuncture according to classical and neuroanatomic principles with electrical stimulation, advice, and exercise. The sham acupuncture group received superficial needling at nonacupuncture points, advice, and exercise, and the final group received advice and exercise only. Symptoms were assessed using the NIH Chronic Prostatitis Symptom Index (NIH-CPSI) and the primary outcome was change in symptoms using this index. All patients receiving electroacupuncture experienced at least a 6 point reduction in the NIH-CPSI total score compared to 16.7% of the sham acupuncture group and 25% of the advice and exercise group. Additionally prostaglandin E2 levels in the urine after prostatic massage decreased in the electroacupuncture group, whereas the levels increased in the other two groups.96 Lee SW and colleagues found that 32 of 44 (72%) CP/CPPS patients receiving acupuncture experienced at least a 6 point decrease in the NIH-CPSI score compared to 21 of 45 (47%) of patients receiving superficial acupuncture at nonacupuncture points.97 Chen and coworkers reported that 10 of 12 CP/CPPS patients who were refractory to antibiotics, α-blockers, antiinflammatory agents, and phytotherapy experienced a greater than 50% reduction in the NIH-CPSI with acupuncture at an average of 33 weeks after treatment.98 A systematic review of acupuncture for the management of labor pain was published in The American Journal of Obstetrics and Gynecology in 2004 and included three RCTs. Two RCTs compared acupuncture with usual care and found that intrapartum acupuncture resulted in lower usage of meperidine and epidural analgesia. One RCT compared acupuncture to superficial needling at nonacupuncture points and found that the classical acupuncture group reported less intrapartum and postpartum pain, requested meperidine and epidural analgesia less often, and required oxytocin augmentation less often.99 Integration with Conventional Pain Medicine Acupuncture therapy is a versatile modality with multiple roles in the contemporary multidisciplinary management of pain. As a safe, cost effective, and evidence-based form of therapy, acupuncture is an ideal

initial input for a variety of subacute and early chronic pain states. As such, its implementation prior to expensive drugs and expensive and potentially dangerous invasive interventions will likely prove beneficial for patients and society. Unfortunately, lack of familiarity with the research establishing acupuncture as safe, cost-effective, and efficacious treatment often results in considering acupuncture as a last resort when all other modalities have failed. A rational approach to treatment that is not driven by economic factors or personal bias ought to use safe, cost-effective, and efficacious therapies early in the therapeutic approach to pain problems, and more risky, expensive, and marginally efficacious therapies later or as “last resorts.” Like any other medical therapy, the results expected from acupuncture for pain control will vary greatly with the severity and chronicity of the underlying condition as well as the underlying health of the patient. Milder pain of more recent onset in a vital young patient can be expected to respond more completely with fewer treatments. A realistic goal for more severe pain of longer duration in chronically debilitated or more frail patients will be partial reduction over a longer course of treatments. Acupuncture can also be useful for the management of ancillary symptoms that accompany chronic pain such as fatigue, secondary dysthymia, or agitation. This being said, acupuncture should not be used as the only treatment for moderate-to-severe depression or other serious psychiatric conditions. Acupuncture treatments are commonly accompanied by a sense of well-being, relaxation, and mild euphoria that can have mild, lasting anxiolytic effects that can be a valuable adjunct in the care of pain patients whose pain is complicated by comorbid fear or anxiety. Side effects that are often encountered in the pharmacologic treatment of pain can also be addressed with acupuncture. For example, nausea, pruritus, dysphoria, and sedation are common side effects of medications used to manage pain. Acupuncture can help diminish these side effects providing for improved patient tolerability and compliance.

Conclusion As understanding of the neurobiologic basis of acupuncture grows, clinical research becomes more sophisticated and patient interest expands, medical acupuncture is becoming more accepted in conventional medical environments. Continued research into the optimal types of acupuncture for specific problems and the most efficient use of acupuncture resources will help clarify the ideal place for acupuncture in the framework of modern medicine. The 20th century witnessed impressive advances in the medical care of acute illnesses such as trauma, infections, and thromboembolic events. Much of the challenge for medicine in the 21st century will be managing complex chronic illnesses of civilization such as diabetes, heart disease, and chronic painful conditions. As a safe, sustainable, cost-effective, and evidence-based therapy for many chronic painful conditions that engenders high patient satisfaction, medical acupuncture is well-suited to play a role in the future of modern medical practice. REFERENCES   1. Reston J. Now, about my operation in Peking. New York Times. 1971 Jul 26:Sect. A.   2. Helms JM. An overview of medical acupuncture. Altern Ther Health Med. 1998;4:35-45.   3. Helms J. Acupuncture Energetics, A Clinical Approach for Physicians. Berkeley: Medical Acupuncture Publishers; 1995:3-17.

Medical Acupuncture  153   4. Unschuld P. Medicine in China. Berkeley: University of California Press; 1985:229-262.   5. Birch S. Understanding Acupuncture. New York: Churchill Livingstone; 1999:43-85.   6. Bauer M. An Interview with Dr. Paul Unschuld, Part 2. Acupuncture Today. 2004;5(8).   7. Karst M, Winterhalter M, Münte S, et al. Auricular acupuncture for dental anxiety: A randomized controlled trial. Anesth Analg. 2007;104:295-300.   8. Kober A, Scheck T, Schubert B, et al. Auricular acupressure as a treatment for anxiety in prehospital transport settings. Anesthesiology. 2003;98:1328-1332.   9. Wang SM, Kain ZN. Auricular acupuncture: A potential treatment for anxiety. Anesth Analg. 2001;92:548-553. 10. Spence DW, Kayumov L, Chen A, et al. Acupuncture increases nocturnal melatonin secretion and reduces insomnia and anxiety: A preliminary report. J Neuropsychiatry Clin Neurosci. 2004;16:19-28. 11. Balk J, Day R, Rosenzweig M, Beriwal S. Pilot, randomized, modified, ­double-blind, placebo-controlled trial of acupuncture for cancer-related fatigue. J Soc Integr Oncol. 2009;7:4-11. 12. Hsieh RL, Wang LY, Lee WC. Additional therapeutic effects of electroacupuncture in conjunction with conventional rehabilitation for patients with first-ever ischaemic stroke. J Rehabil Med. 2007;39:205-211. 13. da Silva JB, Nakamura MU, Cordeiro JA, et al. Acupuncture for dyspepsia in pregnancy: A prospective, randomised, controlled study. Acupunct Med. 2009;27:50-53. 14. Sindrup SH, Otto M, Finnerup NB, Jensen TS: Antidepressants in the treatment of neuropathic pain. Basic Clin Pharmacol Toxicol. 2005;96:399-409. 15. Saarto T, Wiffen PJ. Antidepressants for neuropathic pain. Cochrane Database Syst Rev. 2005;3:CD005454. 16. Villoslada P, Steinman L, Baranzini SE. Systems biology and its application to the understanding of neurological diseases. Ann Neurol. 2009;65:124-139. 17. Huang RS, Ratain MJ. Pharmacogenetics and pharmacogenomics of anticancer agents. CA Cancer J Clin. 2009;59:42-55. 18. Searle R, Hopkins PM. Pharmacogenomic variability and anaesthesia. Br J Anaesth. 2009;103:14-25. 19. Limdi NA, Veenstra DL. Warfarin pharmacogenetics. P ­ harmacotherapy. 2008;28:1084-1097. 20. Witt C, Brinkhaus B, Jena S, et al. Acupuncture in patients with osteoarthritis of the knee: A randomised trial. Lancet. 2005;366:136-143. 21. Scharf HP, Mansmann U, Streitberger K, et al. Acupuncture and knee osteoarthritis: A three-armed randomized trial. Ann Intern Med. 2006;145:12-20. 22. Hui KK, Liu J, Marina O, et al. The integrated response of the human cerebro-cerebellar and limbic systems to acupuncture stimulation at ST 36 as evidenced by fMRI. Neuroimage. 2005;27:479-496. 23. Kou W, Bell JD, Gareus I, et al. Repeated acupuncture treatment affects leukocyte circulation in healthy young male subjects: A randomized ­single-blind two-period crossover study. Brain Behav Immun. 2005;19:318-324. 24. Zhao ZQ. Neural mechanism underlying acupuncture analgesia. Prog Neurobiol. 2008;85:355-375. 25. Kavoussi B, Ross BE. The neuroimmune basis of anti-inflammatory acupuncture. Integr Cancer Ther. 2007;6:251-257. 26. Han JS. Acupuncture and endorphins. Neurosci Lett. 2004;361:258-261. 27. Pyne D, Shenker NG. Demystifying acupuncture. Rheumatology. 2008;47:1132-1136. 28. Melzack R. Evolution of the neuromatrix theory of pain. The Prithvi Raj Lecture: Presented at the Third World Congress of World Institute of Pain, Barcelona 2004. Pain Pract. 2005;5:85-94. 29. Napadow V, Kettner N, Liu J, et al. Hypothalamus and amygdala response to acupuncture stimuli in carpal tunnel syndrome. Pain. 2007;130:254-266. 30. Stux G, Berman B, Pomeranz B. Basics of Acupuncture. New York: Springer-Verlag; 2003:7-27. 31. Langevin HM, Churchill DL, Cipolla MJ. Mechanical signaling through connective tissue: A mechanism for the therapeutic effect of acupuncture. FASEB J. 2001;15:2275-2282.

32. Langevin HM. Connective tissue: A body-wide signaling network? Med Hypotheses. 2006;66:1074-1077. 33. Langevin HM, Churchill DL, Wu J, et al. Evidence of connective tissue involvement in acupuncture. FASEB J. 2002;16:872-874. 34. Langevin HM, Bouffard NA, Churchill DL, Badger GJ. Connective tissue fibroblast response to acupuncture: Dose-dependent effect of bidirectional needle rotation. J Altern Complement Med. 2007;13:355-360. 35. Shah JP, Danoff JV, Desai MJ, et al. Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Arch Phys Med Rehabil. 2008;89:16-23. 36. Simons DG. New views of myofascial trigger points: Etiology and diagnosis. Arch Phys Med Rehabil. 2008;89:157-159. 37. Smith GV, Alon G, Roys SR, et al. Functional MRI determination of a dose-response relationship to lower extremity neuromuscular electrical stimulation in healthy subjects. Exp Brain Res. 2003;150:33-39. 38. Korvenoja A, Huttunen J, Salli E, et al. Activation of multiple cortical areas in response to somatosensory stimulation: Combined magnetoencephalographic and functional magnetic resonance imaging. Hum Brain Mapp. 1999;8:13-27. 39. Moisset X, Bouhassira D. Brain imaging of neuropathic pain. ­Neuroimage. 2007;37:S80-S88. 40. Lewith GT, White PJ, Pariente J. Investigating acupuncture using brain imaging techniques: The current state of play. Evid Based Complement Alternat Med. 2005;2:315-319. 41. Dhond RP, Kettner N, Napadow V. Neuroimaging acupuncture effects in the human brain. J Altern Complement Med. 2007;13:603-616. 42. Liu WC, Feldman SC, Cook DB, et al. fMRI study of acupunctureinduced periaqueductal gray activity in humans. Neuroreport. 2004;15:1937-1940. 43. Neugebauer V, Li W, Bird GC, Han JS. The amygdala and persistent pain. Neuroscientist. 2004;10:221-234. 44. Napadow V, Kettner N, Ryan A, et al. Somatosensory cortical plasticity in carpal tunnel syndrome—A cross-sectional fMRI evaluation. ­Neuroimage. 2006;31:520-530. 45. Napadow V, Liu J, Li M, et al. Somatosensory cortical plasticity in carpal tunnel syndrome treated by acupuncture. Hum Brain Mapp. 2007;28:159-171. 46. Faingold CL. Electrical stimulation therapies for CNS disorders and pain are mediated by competition between different neuronal networks in the brain. Med Hypotheses. 2008;71:668-681. 47. Witt CM, Brinkhaus B, Reinhold T, et al. Efficacy, effectiveness, safety and costs of acupuncture for chronic pain—results of a large research initiative. Acupunct Med. 2006;24:S33-S39. 48. Witt CM, Jena S, Selim D, et al. Pragmatic randomized trial evaluating the clinical and economic effectiveness of acupuncture for chronic low back pain. Am J Epidemiol. 2006;164:487-496. 49. Haake M, Müller HH, Schade-Brittinger C, et al. German acupuncture trials (GERAC) for chronic low back pain: randomized, multicenter, blinded, parallel-group trial with 3 groups. Arch Intern Med. 2007;167: 1892-1898. 50. Wu MT, Sheen JM, Chuang KH, et al. Neuronal specificity of acupuncture response: A fMRI study with electroacupuncture. Neuroimage. 2002;16:1028-1037. 51. Li G, Cheung RT, Ma QY, Yang ES. Visual cortical activations on fMRI upon stimulation of the vision-implicated acupoints. Neuroreport. 2003;14:669-673. 52. Shiotani A, Tatewaki M, Hoshino E, et al. Effects of electroacupuncture on gastric myoelectrical activity in healthy humans. Neurogastroenterol Motil. 2004;16:293-298. 53. Kroeling P, Gross AR, Goldsmith CH, et al. A Cochrane review of electrotherapy for mechanical neck disorders. Spine. 2005;30:E641-E648. 54. Peloso P, Gross A, Haines T, et al. Medicinal and injection therapies for mechanical neck disorders. Cochrane Database Syst Rev. 2007;3:CD000319. 55. van Tulder MW, Koes B, Seitsalo S, et al. Outcome of invasive treatment modalities on back pain and sciatica: An evidence-based review. Eur Spine J. 2006;15:S82-S92.

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154  Complementary and Alternative Medical Procedures 56. van Tulder MW, Koes B, Malmivaara A. Outcome of non-invasive treatment modalities on back pain: An evidence-based review. Eur Spine J. 2006;15:S64-S81. 57. Ernst E, White AR. Prospective studies of the safety of acupuncture: A systematic review. Am J Med. 2001;110:481-485. 58. Witt CM, Pach D, Brinkhaus B, et al. Safety of acupuncture: Results of a prospective observational study with 229,230 patients and introduction of a medical information and consent form. Forsch Komplementmed. 2009;16:91-97. 59. Wonderling D, Vickers AJ, Grieve R, et al. Cost effectiveness analysis of a randomised trial of acupuncture for chronic headache in primary care. BMJ. 2004;328:747. 60. Evans KW, Boan JA, Evans JL, Shuaib A. Economic evaluation of oral sumatriptan compared with oral caffeine/ergotamine for migraine. ­Pharmacoeconomics. 1997;12:565-577. 61. Willich SN, Reinhold T, Selim D, et al. Cost-effectiveness of acupuncture treatment in patients with chronic neck pain. Pain. 2006;125:107-113. 62. Ratcliffe J, Thomas KJ, MacPherson H, Brazier J. A randomised controlled trial of acupuncture care for persistent low back pain: Cost effectiveness analysis. BMJ. 2006;333(7569):626. 63. van Weel C, Knottnerus JA. Evidence-based interventions and comprehensive treatment. Lancet. 1999;353:916-918. 64. Mant D. Can randomised trials inform clinical decisions about individual patients? Lancet. 1999;353:743-746. 65. Feinstein AR, Horwitz RI. Problems in the ‘‘evidence’’ of ‘‘evidencebased medicine’’. Am J Med. 1997;103:529-535. 66. Hotopf M. The pragmatic randomised controlled trial. Adv Psychiatr Treat. 2002;8:326-333. 67. Katon W, Von Korff M, Lin E, et al. Stepped collaborative care for primary care patients with persistent symptoms of depression: a randomized trial. Arch Gen Psych. 1999;56:1109-1115. 68. Hróbjartsson A, Gøtzsche PC. Placebo treatment versus no treatment. Cochrane Database Syst Rev. 2003;1:CD003974. 69. Serruys PW, Morice MC, Kappetein AP. Percutaneous coronary intervention versus coronary-artery bypass grafting for severe coronary artery disease. N Engl J Med. 2009;360:961-972. 70. Furlan AD, van Tulder MW, Cherkin DC, et al. Acupuncture and dry-needling for low back pain. Cochrane Database Syst Rev. 2005;1: CD001351. 71. Brinkhaus B, Witt CM, Jena S, et al. Acupuncture in patients with chronic low back pain: a randomized controlled trial. Arch Intern Med. 2006;166:450-457. 72. Trinh KV, Graham N, Gross AR, et al. Acupuncture for neck disorders. Cochrane Database Syst Rev. 2006;3:CD004870. 73. Linde K, Allais G, Brinkhaus B, et al. Acupuncture for migraine prophylaxis. Cochrane Database Syst Rev. 2009;1:CD001218. 74. Linde K, Allais G, Brinkhaus B, et al. Acupuncture for tension-type headache. Cochrane Database Syst Rev. 2009;1:CD007587. 75. Endres HG, Diener HC, Molsberger A. Role of acupuncture in the treatment of migraine. Expert Rev Neurother. 2007;7:1121-1134. 76. Li Y, Liang F, Yang X, et al. Acupuncture for treating acute attacks of migraine: A randomized controlled trial. Headache. 2009;49:805-816. 77. Melchart D, Thormaehlen J, Hager S, et al. Acupuncture versus placebo versus sumatriptan for early treatment of migraine attacks: A randomized controlled trial. J Intern Med. 2003;253:181-188. 78. White A, Foster NE, Cummings M, et al. Acupuncture treatment for chronic knee pain: A systematic review. Rheumatology. 2007;46:384-390.

79. Manheimer E, Linde K, Lao L, et al. Meta-analysis: Acupuncture for osteoarthritis of the knee. Ann Intern Med. 2007;146:868-877. 80. Green S, Buchbinder R, Hetrick S. Acupuncture for shoulder pain. Cochrane Database Syst Rev. 2005;2:CD005319. 81. Green S, Buchbinder R, Hetrick S. Physiotherapy interventions for shoulder pain. Cochrane Database Syst Rev. 2003;2:CD004258. 82. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain. Cochrane Database Syst Rev. 2003;1:CD004016. 83. Guerra de Hoyos JA. Andrés Martín Mdel C, Bassas y Baena de Leon E, et al. Randomised trial of long term effect of acupuncture for shoulder pain. Pain. 2004;112:289-298. 84. Johansson KM, Adolfsson LE, Foldevi MO. Effects of acupuncture versus ultrasound in patients with impingement syndrome: Randomized clinical trial. Phys Ther. 2005;85:490-501. 85. Vas J, Ortega C, Olmo V, et al. Single-point acupuncture and physiotherapy for the treatment of painful shoulder: A multicentre randomized controlled trial. Rheumatology. 2008;47:887-893. 86. Trinh KV, Phillips SD, Ho E, Damsma K. Acupuncture for the alleviation of lateral epicondyle pain: A systematic review. Rheumatology. 2004;43:1085-1090. 87. Trudel D, Duley J, Zastrow I, et al. Rehabilitation for patients with lateral epicondylitis: A systematic review. J Hand Ther. 2004;17:243-266. 88. Stener-Victorin E, Kruse-Smidje C, Jung K. Comparison between electro-acupuncture and hydrotherapy, both in combination with patient education and patient education alone, on the symptomatic treatment of osteoarthritis of the hip. Clin J Pain. 2004;20:179-185. 89. Witt CM, Jena S, Brinkhaus B, et al. Acupuncture in patients with osteoarthritis of the knee or hip: a randomized, controlled trial with an additional nonrandomized arm. Arthritis Rheum. 2006;54:3485-3493. 90. Mayhew E, Ernst E. Acupuncture for fibromyalgia—a systematic review of randomized clinical trials. Rheumatology. 2007;46:801-804. 91. Rosted P. Practical recommendations for the use of acupuncture in the treatment of temporomandibular disorders based on the outcome of published controlled studies. Oral Dis. 2001;7:109-115. 92. Smith P, Mosscrop D, Davies S, et al. The efficacy of acupuncture in the treatment of temporomandibular joint myofascial pain: A randomised controlled trial. J Dent. 2007;35:259. 93. Sun Y, Gan TJ, Dubose JW, et al. Acupuncture and related techniques for postoperative pain: A systematic review of randomized controlled trials. Br J Anaesth. 2008;101:151-160. 94. Usichenko TI, Dinse M, Hermsen M, et al. Auricular acupuncture for pain relief after total hip arthroplasty—a randomized controlled study. Pain. 2005;114:320-327. 95. Taguchi A, Sharma N, Ali SZ, et al. The effect of auricular acupuncture on anaesthesia with desflurane. Anaesthesia. 2002;57:1159-1163. 96. Lee SH, Lee BC. Electroacupuncture relieves pain in men with chronic prostatitis/chronic pelvic pain syndrome: Three-arm randomized trial. Urology. 2009;73:1036-1041. 97. Lee SW, Liong ML, Yuen KH, et al. Acupuncture versus sham acupuncture for chronic prostatitis/chronic pelvic pain. Am J Med. 2008;121:79:e1-e7. 98. Chen R, Nickel JC. Acupuncture ameliorates symptoms in men with chronic prostatitis/chronic pelvic pain syndrome. Urology. 2003; 61:1156-1159. 99. Skilnand E, Fossen D, Heiberg E. Acupuncture in the management of pain in labor. Acta Obstet Gynecol Scand. 2002;81:943-948.

Osteopathic Manipulative Medicine: A Functional Approach to Pain

18

Stevan Walkowski, DO, and Robert Baker, DO

“Nature applies to you the switch of pain when her mandates are disregarded, and when you feel the smarting of her switch, do not pour drugs into your stomachs, but let a skillful engineer adjust your human machine, so that every part works with Nature’s requirements.”1 The practice of osteopathic medicine is the practice of a complete system of medicine with deep historical and philosophical underpinnings. As osteopathic physicians, we are given the unique opportunity to use all means available to help our patients, from technological testing to surgical procedures and pharmaceuticals. Additionally, we are given the tools to affect the body’s physiology through manipulative therapies. We are taught from our first days in medical school how to use our hands to diagnose and treat dysfunction within the musculoskeletal system whether it is expressed as structural problems or more systemic problems. By restoring function to the tissue, we are restoring health, and because pain is a symptom of dysfunction within the organism, we have the opportunity to provide relief from suffering. Osteopathic manipulative medicine has an application in all specialties of medicine—from family practice to cardiothoracic surgery—because musculoskeletal pain and visceral distress exhibit somatic dysfunction and are amenable to osteopathic treatment. This chapter is designed to be an introduction to the practice of osteopathic manipulative medicine. Although it is possible to read about diagnosis and treatment principles and begin to apply them in your practice, the study of this body of knowledge is best accomplished through application and direction within a formal course of study. The intention of this chapter is to provide an overview of the history, principles, and examples of common diagnosis and treatments in osteopathic manipulative medicine. Further resources will be introduced later in the chapter for the reader to explore and expand on the knowledge and information described here.

History of Osteopathy Osteopathy has had a rich and varied history. One of the unique aspects of this profession is the importance of understanding its roots and the relationship of its roots to the present day practice of osteopathic medicine. It is only through understanding the totality of osteopathic medicine can one begin to appreciate fully the impact of osteopathic manipulative medicine. The heroes and founders of the osteopathic profession are unique and they bear

witness to the tenacity of a belief in a style of practice different from the “medicine of the day.” Truly an American practice of medicine, osteopathy began on June 22, 1874 in Kansas when Andrew Taylor Still, MD “flung to the breeze the banner of osteopathy”1 and “like an explorer trimmed [his] sail…”.1 A.T. Still was born in 1828 in Jonesboro, Virginia, but he grew up in Missouri as the son of a Methodist minister. Many stories surround the early years of Dr. Still, but little historical evidence is documented. As a Methodist minister, his father was a “circuit rider,” a preacher who would travel out to the edges of the frontier, settle his family, and provide religious service to the pioneers of that day. Although he would also do some missionary work to the indigenous people, conversion was rarely successful. Young Andrew was known to have spoken with the Native Americans around his father’s settlement and was said to have learned about the practice of herbal medicine from them. He was also known to have taken some skeletal remains from the burial grounds and with them began his study of anatomy. As he grew older and the debate around slave states and free states grew, he was a noted abolitionist and later joined the Kansas militia as sides were taken in the early days of the Civil War. Following his tour of duty in the Kansas militia, he returned home and began the study of medicine as it was practiced in the late 1800s. Practices such as bleeding, administration of purgatives and cathartics, including arsenic and mercury, were common and considered standard of care at that time. This “heroic medicine” was mainly directed at suppressing symptoms and was practiced prior to the advent of the microbial orientation of disease or the understanding of much of the pathophysiology that we take for granted today. He became an accomplished physician by apprenticeship as was the custom and was awarded the title of Medical Doctor. An important event occurred in 1864 when a meningitis outbreak took the lives of three of Still’s children. This devastated Andrew and he “blamed the gross ignorance of the medical profession for the deaths of his children.”2 This tragedy created an alarming sense of helplessness in Andrew and from then on he was determined to find better methods of healing.2 After a prolonged episode of depression and fasting, along with meditation and prayer, he came to the realization that the 155

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human form was a perfect reflection of the divinity that created it with the further realization that all of the natural elements of healing were present in the human body, and needed a physician only to release them. He reasoned that any being so created would have contained within it all of the substances it needs to heal itself and that the mechanical structure of the body must have a significant impact on its function. As Still’s most prominent quote said “To find health should be the object of the doctor. Anyone can find disease.”3 It was also the object of the physician to understand every aspect of human anatomy because it is only through understanding of anatomy that an accurate assessment of the healthy functioning of the body could be ascertained. This new science, Dr. Still called “osteopathy”, because it was the study of the relationship that the osseous structure and its interrelationships had on health. He advocated abandoning all use of drugs in favor of dietary, spiritual, and mechanical functional treatment. During the late 1880s, word of Dr. Still’s successes was traveling far, and with it the desire by many patients to be seen. The local train station in Kirksville at the time had to increase the number of stops into Kirksville because of so many patients flocking there in hope of relief. Because of this growing success, A.T. Still began to attract the attention of other physicians who wanted to learn this skill that seemed to be healing those who were previously found to be beyond repair. In 1892, he started the American School of Osteopathy in Kirksville, Missouri, and began teaching the first class of 17 students, of which notably three were women. The major system of study was anatomic dissection and the study of manual therapies designed to improve the overall functioning of the human body, allowing it to move toward its natural state of health. One of these first 17 students was Arthur Hildreth, a friend of the Still family, who went on to great success and eventually wrote a book about his great teacher. In the book he says of Dr. Still: “I wish it were in my power to describe in a simple, practical way some of his most outstanding technics. Not only the methods he used but also his own individual way of explaining what he did,” also, “Dr. Still’s technique was marvelous, often beyond our comprehension. He seemed to do everything so easily we wondered how he could accomplish so much.”4 This same Dr. Hildreth was the pioneer who led the charge in many states to gain practice rights for this new method of healing called ”osteopathy”. Osteopathy has suffered minor setbacks in its history since the time of Dr. Still, but also many successes. There are now 25 schools of osteopathic medicine and the total number of DOs (doctors of osteopathy) totals more than 61,000. There are 18 specialty boards and the practice of medicine is unrestricted in each of the fifty states in the United States. Osteopathy is a recognized form of medicine in 44 countries world-wide with unlimited practice rights and recognized in another 8 countries with practices limited to osteopathic manipulative medicine. At present, the practice of osteopathic manipulative medicine is both a specialty practice and considered an integral part of any other specialty in osteopathic medicine. Osteopathic manipulative medicine is taught at all of the osteopathic medical schools in the first 2 years and is reinforced in the clinical third and fourth years. The American Osteopathic Association has listed it as the first Core Competency requirement in all osteopathic residency programs, and it is the intent of the AOA to ensure that the practice of osteopathic manipulative medicine be integrated into all residency training programs and all clinical practices of osteopathic medicine. Although it is part of a complete system of medicine and is applicable for both musculoskeletal

problems and internal systemic dysfunctional issues, this chapter will largely deal with the use of manipulative medicine in pain.

Principles of Osteopathic Medicine Osteopathic medicine is the only system of medicine that has clearly established principles guiding its practice. The principles, as distilled from the writings of A.T. Still, M.D., include (1) the body is a unit; (2) structure and function are interrelated; (3) the body has the innate ability to heal itself; (4) rational practice of medicine must take these principles into account. These tenets of osteopathy are easily developed to encompass a holistic treatment paradigm that characterizes osteopathy in the 21st century. That the body should be considered as a unified whole as opposed to a summation of its parts is central to the first tenet. Additionally, one must consider the individual as an extension of his entire environment: social, family, environmental, nutritional, psychospiritual. It must be recognized that each aspect of his existence plays as significant role in the maintenance of his health and must be addressed if health is to be restored and maintained. The interrelationship between structure and function seems central to the practice of osteopathic manipulative medicine in particular. More significantly, perhaps, is the realization that the structure of the body and its function are intrinsically, reciprocally, and inextricably connected; that one cannot be altered without affecting the other and that the health of the organism could easily be affected by limitations in its function. Understanding that the body has the innate ability for self-­ healing is common knowledge today as we understand many examples of the homeostatic mechanisms that are present in many regulatory functions that the body possesses. This tenet implies, however, that the natural and innate state of the body is health, that the organism will instinctively move toward health, and that left unimpeded and supported, will continue its movement toward health throughout its lifetime. This concept is in significant opposition to the common method of pharmaceutical healing wherein all ills are seen as a result of the excess of something and what is most needed is medication that is designed to suppress whatever has invaded the organism or spun out of control. This tenet of self-­ healing supports the notion that by providing the right environment, structure, and milieu, the body will naturally take that information and use it instinctually in its eternal movement toward health. Although this concept may have been medical heresy in 1874, none of these tenets seems far-fetched, even in today’s scientific environment and to say that rational treatment of disease requires an adherence to the aforementioned tenets follows easily. However, if one is to consider the veracity of these principles, then it is incumbent on all physicians to consider, at each turn, with each diagnostic and treatment choice, what among the range of possible options holds the most benefit, with the lowest risk, and honors the principles described earlier. What are the limits of all available treatments and which is the one with the most promise of being resonant with the health of the individual and, at the same time, which treatment holds the lowest risk?

Diagnostic Principles Because osteopathic manipulative treatment is aimed at restoration of function, the diagnosis of dysfunction within the somatic system is a crucial starting point. As Dr. Still’s writing was ripe with

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concepts and barren with practice, the clarification and development of these topics is ongoing within the osteopathic profession. The primary structural diagnosis in osteopathic manipulative medicine is “somatic dysfunction.” This is defined by the AOA glossary of terms as “impaired or altered function of related components of the somatic (body framework) system: skeletal, arthrodial, and myofascial structures and their related vascular, lymphatic, and neural elements.”5 This broad definition is important for two reasons: (1) it creates a definitive concept around a palpatory experience and (2) it extends the scope of dysfunction to a zone greater than that of the neuromusculoskeletal system, that of the visceral and cellular functioning of the human organism. This diagnosis is based on palpatory findings within the musculoskeletal system. The classic acronym for establishing a diagnosis of somatic dysfunction is STAR, which stands for sensitivity, tissue texture change, asymmetry of palpatory landmarks, and restriction of motion. Sensitivity may be identified as the patient’s experience of nociception to palpation, that is, tenderness, although sensitivity could be identified as hypalgesia, dysesthesia, or paresthesia. Tissue texture change is the appreciation of a palpatory difference of resilience of the examined tissue when compared to the surrounding area or an area of mirror image tissue; zones superior, inferior, or contralateral to those examined. Descriptors such as “boggy”, “ropy”, “banded” are commonly used to document alterations from the patient’s individual baseline reference. Asymmetry of palpatory landmarks is easily appreciated by the beginner at shoulder heights, iliac crest heights, or relative lengths of the lower extremities at the medial malleoli. Less obvious are discrepancies between the heights of the occipital condyles, anterior and posterior superior iliac spines, or pubic tubercles. More difficult to appreciate are prominences of rib angles, transverse processes of the vertebral segments, and the relative depths of the sacral sulci. Restriction of motion is the final examination criteria for the diagnosis of somatic dysfunction. This restriction of motion is generally very small and limited to one segment or joint but can extend to surrounding segments. Through the process of segmental definition, a practitioner evaluates a patient with greater and greater tissue specificity until a segmental diagnosis such as T3 flexed, rotated right, and side-bent right is determined. These diagnoses are based upon the normal motions of the regions being examined and are named according to their respective motions of ease rather than restriction. Therefore, in the example, examination would have found the third thoracic vertebrae was relatively restricted in its motion of extension, rotation to the left, and side-bending left when compared to the segments T2 and T4. Diagnostic Process In addition to conventional medical diagnostic procedures, palpatory examination leading to segmental diagnosis of somatic dysfunction is essential to the practice of osteopathic manipulative medicine. Typically, the process of coming to a diagnosis usually involves some measure of palpatory screen, scan, and finally, segmental definition. Screening is the process of palpation and movement designed to answer the question, “Is there a problem?” Scanning answers the question, “Where is the problem?” and segmental definition answers the question, “What is the problem?”6 The screening structural examination is a rapid assessment of tissue texture and motion asymmetries throughout the body, evaluating the differences in tissue texture and motion in the major regions of the body: head, cervical, thoracic, ribs, lumbar, sacropel­ vis, upper extremities, and lower extremities. This is accomplished by broad-based palpation using an open, flat hand to assess tissue

tension in two of each of these regions and determine if there is a differential tension at any of them. For instance, screening examination of the lumbar spine consists of a flat hand placement over the upper lumbar region and lower lumbar region. If there is a difference in tension between those two regions, that difference is noted. Similarly, palpation of the upper extremity checks the tension bilaterally in the upper (humeral) arm and separately at the lower (radio-ulnar) arm. Regional motion is assessed by testing for the relative extent of passive (practitioner-directed) motion capacity in two planes and noting the presence of asymmetry. For example, the cervical spine is tested by slowly rotating the head on the cervical spine passively to the right and left and noting differences in the endpoint of motion. If the spine is capable of rotating more to the left than the right, that difference is noted. Typically, two separate motions are used to screen any region just as two areas are palpated in any region. Again, in the cervical spine, rotation and side-­bending are typically tested. A presence of asymmetry in tissue tension and motion in any of the regions is considered prima facie evidence of somatic dysfunction and demands a scanning evaluation. The scanning examination is one that narrows the finding of somatic dysfunction to a segment, rib, or joint. This is accomplished by a more focused palpation over the region assessing changes in tissue texture that are more specific to the region involved. For instance in the thoracic spine, palpation along the zone of the transverse processes, segment by segment, will help to identify the segment that is dysfunctional, usually by noting a firmness of the surrounding tissue as compared to the segmental transverse process above and below it. This finding is then confirmed through motion testing by initiating passive side-bending or rotation in the thoracic spine and then observing the tissue response to that motion and comparing that response to motion in the segments above and below it. For example, after screening the thoracic spine and finding it to be dysfunctional, a scan is performed and the 5th thoracic segment displays increased tissue tension at the region of the transverse process when compared to the transverse processes above and below it. With the patient’s arms crossed (to eliminate unconscious external stabilization), the trunk is side-bent to the left and an assessment of ease or bind at the 5th thoracic segment is identified as compared to the segments above and below. If restriction to motion is identified with left side-bending, there will be ease to right side-bending of the thoracic spine. Typically, a restriction to motion is more easily appreciated on palpation, but conventionally, the segment is always described in its direction of ease; therefore, the 5th thoracic segment with restriction to side-bending to the left is described as “side-bent right.” The choice of side-bending as a test is completely arbitrary here and passive rotation could just as easily have been demonstrated. The findings of segmental tissue texture change and motion asymmetry determine a positive scan and the next step, segmental definition, must be accomplished if any treatment is to be considered (Fig. 18-1). Segmental definition is the process of finely tuning one’s scan and focusing palpation and motion testing to account for all possible motion characteristics that occur at the particular segment or joint. To continue our example of the 5th thoracic vertebrae, we identified that motion ease is palpated in lateral side-bending to the right.3 Additionally, we must further check rotation right and left, flexion and extension, anterior or posterior translation, cephalad or caudad translation, or ease in response to the respiratory cycle of inhalation or exhalation. Again, this testing is done passively with the operator moving the patient in all of the aforementioned planes of motion with a palpating hand checking for tissue response to that movement. This provides the most accurate and detailed

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Figure 18-1  Scanning the thoracic region. This figure demonstrates the ­position for determining segmental response to regional rotation of the thoracic spine.

type of definition for a vertebral segment. Segmental definition of joints of the extremities is a natural extension of the scan for that region. Because motion restriction is detected asymmetrically in the extremities, that motion is more definitively described according to the major motions, but also the minor or secondary motions, such as glide and translation. While these secondary motions are significant in the vertebral column, these subtler motions in the extremities often hold the key to defining dysfunction and, hence, treating it. This style of diagnosing somatic dysfunction is but one method of approach to this problem. It is a simple, yet comprehensive approach to the entire body. There are as many approaches to defining somatic dysfunction as there are practitioners of osteopathic manipulative medicine, but they each contain some portion of the steps elucidated herein. What is simple is not always easy. Palpating for these tissue texture changes and motion characteristics seems simple when described, but the psychomotor skill of applying these techniques is extremely difficult to begin to appreciate and takes many years to master. As in many other aspects of medicine, the learning process continues until death. Osteopathy has the unique attribute of revealing itself through its patients to the practitioner, if he or she approaches it with open eyes, an open heart, and thinking fingers. My patients teach me every day, and new clues to a greater appreciation of osteopathy are revealed to me, unexpectedly, enriching my experience and my ability to help them.

Treatment Osteopathic manipulative treatment is divided into two main types: direct and indirect. Direct techniques are those in which an operator moves a segment or joint in a direction toward its barrier to

motion and uses an internal or externally applied force to create movement through that barrier to restore normal motion and function. Examples of direct treatment include: muscle energy technique, high-velocity low amplitude technique, and direct myofascial release technique. Conversely, an indirect treatment moves a segment in a direction away from its barrier and allows for a spontaneous correction or release to restore normal motion and function. Examples of indirect treatment include: strain counterstrain technique, functional methods technique, and indirect myofascial release technique. Inherent in these descriptions is the barrier concept. This much debated concept is a direct result of palpatory experience in segmental definition (Fig. 18-2). One model of the barrier concept states that there exists within any segment or joint, a neutral zone in which all of the forces that normally impinge on that segment or joint are equal and balanced. There is a zone around that neutral area that represents the entirety of the normal range of motion that segment or joint possesses. Any motion that segment or joint performs is met with increasing resistance as it approaches its endpoint of motion or barrier. Some definitions of the barrier include distinctions of motion that describe the barrier to passive motion versus the barrier to active motion, or the barrier that exists between the endpoint of passive motion and the barrier that occurs at the limitation of bony resistance of the skeleton. Another important part of the barrier concept is that of a pathologic neutral. When a joint or segment is functioning fully, its neutral position of rest is balanced within its endpoints of motion. When one of the functional endpoints of motion or barriers have been changed through dysfunction, then a new balance point is established that is still neutral in relation to its total potential of function. That change in the neutral is palpable in structural diagnosis as somatic dysfunction. The restriction to motion in one or more planes of motion creates palpatory findings that are commensurate with the definitions of dysfunction. As an example of direct technique, in the case of T5 flexed, rotated right and side-bent right, by definition, it is named for its positions of ease of motion. Conversely, this means that its directions of restriction are extension, rotation left, and side-bending left. In a direct technique, the segment is moved into its directions of restriction and an activating force is applied to move it through that barrier. An indirect technique is applied by moving the segment into its direction of ease of motion and the intrinsic physiologic forces are used to allow for a release of the dysfunction. In both cases, following treatment, the segment is rechecked to ensure that a change to a more functional state has been achieved.

Muscle Energy Treatment: Lumbar Muscle energy treatment was developed by Fred Mitchell, Sr., DO, as a way to approach problems directly without high-velocity, lowamplitude thrusting.7 This is a direct technique in which the operator moves the dysfunctional segment toward its restrictive barrier and then stabilizes it while the patient applies an isometric contraction away from the barrier. This contraction is held for 3 to 5 seconds and the patient is instructed to discontinue the contraction. At that point, the operator readjusts the position of the segment to accommodate for the muscle relaxation and lengthening that has occurred, and moves the segment into a new barrier. This sequence is repeated until maximum improvement in the segmental findings is achieved. The advantage of this technique is that the force that is applied is generated by the patient and monitored by the physician.

Osteopathic Manipulative Medicine: A Functional Approach to Pain  159 AB

PB

O

PB

AB

O

PB

AB

O

PB

AB

Normal range of motion no somatic dysfunction (SD)

AB

PB Motion loss

PB RB

Normal motion

SD

AB

PB RB

O O

PB

AB

AB

PB RB

O O

PB

AB

PB

AB

Normal motion

SD

AB

PB RB

PB

O O

O O

RB

Normal motion

SD

AB

PB AB

O Figure 18-2  Somatic dysfunction in a single plane: three methods ­illustrating the “restrictive barrier” (the restrainer): AB, Anatomic barrier; PB, Physiologic barrier; RB, Restrictive barrier; SD, Somatic dysfunction.

Dr. Fred Mitchell, Jr, DO, who wrote extensively about his father’s technique, explained that the anatomy in a patient’s own (body) was more precisely and intimately known to the patient’s muscles than they could be to any examiner. For this reason he said, his father chose to use the energy of the patient’s muscles instead of his own for the corrective forces.7 This alleviates the danger or unnecessarily overzealous application of an externally applied force. Difficulties with this procedure usually surround the localization of force by the practitioner, lack of stabilization against the isometric contraction on the part of the physician, and too great a force applied by the patient. The force applied need only be great enough to engage the tissues at the level of the localized, treated segment. Too great a force can become too diffuse and difficult to localize around the segment, it may also be too strong to oppose by the physician. The treated segment must be stabilized in its position against the barrier and if that stabilization is compromised because the physician is trembling against the force of the patient, it will be impossible to maintain a stable position at the barrier. Muscle energy technique, when properly applied, should not look like a wrestling match. The lumbar spine is identified as the lower five vertebrae resting on the sacrum. These are large vertebrae with no rib attachments. Primary motions at these segments include flexion, extension, side-bending, and rotation. The intervertebral discs support the vertebrae, providing both a cushion for shock absorption and a stable, yet flexible interface between the segments, allowing for movement. The remainder of the vertebrae include a pedicle and spinous process creating the spinal canal; transverse processes bilaterally and articular processes above and below the transverse process that create functional joints with the spinal segments superior and inferior to it. These processes form the zygapophyseal or facet joints, true synovial joints in the lumbar spine. Between the pedicles of each of the vertebral segments course the peripheral spinal nerve roots.8 Pain in the lumbar spine is common and multifactorial.9 It is beyond the scope of this chapter to discuss all of the possible causes of back pain; more importantly, there is much speculation about the true etiologies of any of these types of pain. Common pathologies occurring in the lumbar spine that can easily affect the function of the region include: osteoarthritis, herniated nucleus pulposus, inflammatory arthropathy, spondylolisthesis, spondylosis, and ligamentous strain. Although each of these problems has its unique presentation, they each have the capacity to express themselves as a functional limitation of that region, exhibiting signs of somatic dysfunction. Disruption of the normal integrity of the musculoligamentous structures of the axial spine in any location can result in muscular hypertonicity. Because this hypertonicity is usually asymmetrical and is generally restrictive in motion of the spine, diagnosis of tissue texture differences and resultant motion asymmetry is quickly identified. Important in the diagnosis of somatic dysfunction at any location is the appreciation of the anatomic and subsequent physiologic influences any dysfunction can have at local, adjacent regions or distal regions, whether by myofascial continuity or neural irritability. Important influences that extend from lumbar dysfunction include regional influences. Lumbar dysfunction with its requisite biomechanical changes can affect segments locally adjacent. Because of the physiologic differences between the regions of the axial spine, dysfunction in the lumbar region can influence the appearance of dysfunction in the thoracic spine and sacropelvis and vice versa. As a result of normal physiologic relationships within the viscera and their relationship to the lumbar region anatomically,

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functions of those viscera can be affected, especially the viscera of the lower pelvis including the large intestine, sigmoid colon, rectum, and pelvic organs. Although this is partly due to the direct effect that a change in normal biomechanics can have on involuntary motions such as those associated with respiration, some of the effect is due to a reflex influence of the somatic system on the autonomic nervous system in the levels of the spine that are affected. In this case, T12 to L2 are most closely associated with the sympathetic cell bodies that provide autonomic influence to the colon below splenic flexure and other pelvic organs. In this way, osteopathic manipulative medicine extends beyond the realm of musculoskeletal pain management and becomes part of a complete system of medicine in which its application begins to influence the visceral function and ultimately the metabolic health of the organism.10 At this point the encompassing definition of “somatic dysfunction” becomes actualized in its application of treatment. Beginning with muscle energy treatment of the lumbar spine, let us assume that the practitioner has previously performed a structural screening examination, scanning examination, and obtained a segmental definition of L4 flexed, rotated, and side-bent to the right. According to the previous discussion this implies ease in the direction of diagnosis and restriction in the opposite directions. Therefore, its motions are restricted at L4 in extension, rotation, and side-bending to the left. Any manner of positioning designed to activate that segment at its points of restriction is appropriate, but for the purpose of this description of treatment, the seated position will be used. Because the nature of this treatment is to provide resistance against the patient’s activating force in an isometric contraction, it is important to consider how one will stabilize the body of the patient while monitoring tissue changes at the dysfunctional segment. Proper body mechanics and choice of positioning allows for the use of as many core trunk muscles of the physician for stabilization and fewer of the muscles of the appendicular skeleton that tend to be shorter and quicker to fatigue. In this case, the patient is seated on the table and the physician is standing behind her on the side of her side-bending restriction. The height of the table or chair is selected to maximize the physician’s ability to apply an adequate counterforce in side-bending by bringing his axilla as close to the superior aspect of his patient’s shoulder on the side of side-­bending restriction. The opposite hand is used to palpate the tissue at the dysfunctional segment and monitor for specific localization of forces into that segmental region. The physician grasps the opposite shoulder by placing his arm across the anterior cervical thoracic junction of the patient and holds the patient snugly. He moves the patient’s trunk passively until the position of restriction is palpated at the previously identified segmental level, which in this case means rotating her trunk to the left and side-bending to the left with lumbar extension until the force of these motions is palpated at L4. The accuracy of the localization of these forces is crucial to the effective application of these techniques (Fig. 18-3). Too little motion and the forces will be localized superior to the segmental region, too much motion and the forces will be directed at a level inferior to the dysfunctional segment. When localization is achieved, the patient is asked to attempt to side-bend and rotate away from the position that she has been put into by the physician. In this case, the patient is directed to, “gently turn to the right.” Generally, only one direction of motion is necessary to activate the force sufficiently to achieve an effect at the dysfunctional segment. Because of normal spinal mechanics, motion in one of the cardinal directions of the spine will affect motion in all the other planes where motion is engaged, so by asking the patient

Figure 18-3  Position for seated muscle energy procedure in the lumbar spine.

only to rotate, side-bending and flexion are normally engaged. The force of the isometric contraction must be palpated at the level of the dysfunctional segment. The localized isometric contraction is held for 3 to 5 seconds and then the patient is asked to stop turning, or to relax. A moment is given to appreciate the relaxation in the tissues and then the segment is moved into its next restrictive barrier, in this case, slightly further rotated left, side-bent left, and extended. This sequence is repeated as many times as it is needed to effect maximal change, but generally this occurs within five repetitions. At that point, the patient is slowly and gently returned to physiologic neutral, and the dysfunctional segment is checked again for improvement in tissue texture and motion. Impediments to the successful application of any of these techniques usually stem from an inaccuracy in the diagnosis or inappropriately applied technique. Whereas an inaccuracy in diagnosis may result from a mistake in interpretation of palpatory findings, more commonly there is a lack of appreciation for the complexity of dysfunctional findings and a missed diagnosis of dysfunction in a seemingly unrelated region that is critical in maintaining the dysfunction that is erroneously being treated as primary. For example, the lumbar dysfunction may be a secondary result of a primary dysfunction in the sacrum. Unless that sacral dysfunction is recognized and treated, the lumbar segment may resolve incompletely or return quickly after treatment. Other common mistakes in muscle energy treatment resulting in lack of complete resolution include, isometric forces too strong or too weak, lack of accurate stabilization resulting in irregular movements during isometric contraction, or returning the patient to a neutral position too quickly. Muscle energy treatment is easy to apply to all regions of the body although the lumbar region is demonstrated here. Wherever one can identify a structural diagnosis in which one or more planes of motion are restricted, the patient can always be moved into the

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edge of that restriction and with a series of isometric contractions, change the presence of that barrier. This includes all of the axial skeleton and appendicular skeleton. The physiology of muscle energy treatment is suspected to be an activation of intramuscular proprioceptive fibers called Golgi tendon organs.11 These sensory units are found at the musculotendinous junctions and, when activated, will reflexively cause the motor units to temporarily shut down and relax the muscle tissue. They are thought to have a protective function against overstretching the muscle. By placing the muscle in a position of restriction and then having the patient isometrically contract, these fibers are thought to be activated and then reflexively allow for muscle relaxation. After the next point of restriction or barrier is achieved, the process is repeated until the dysfunction is resolved. Muscle energy treatment is very effective in conditions where an obvious muscular hypertonicity is palpated. It may be too vigorous treatment in an acute injury, although there are no contraindications for its use in that situation. In general, muscle energy treatment is well tolerated by patients and extremely effective in its treatment of somatic dysfunction.

Strain Counterstrain Treatment: Cervical Region Strain counterstrain treatment, or spontaneous release by positioning, was developed by Lawrence Jones, DO, and first described in the literature in 1964. The initial discovery of this technique is derived from a patient encounter wherein Dr. Jones was having difficulty treating his patient’s low back pain. After treating him several times unsuccessfully, he asked his patient if there was any position that could be comfortable for him. As the patient assumed that position on the treatment table, Dr. Jones began to prop his extremities and support his spine. After achieving that position of comfort, Dr. Jones left the room and went about treating other patients. When he returned to the treatment room, his patient was asleep. He quietly woke him to find that he was pain free. After slowly removing his supports and helping him sit up from the treatment table, the patient exclaimed that he felt better than he had been in months. Shocked at the dramatic improvement, Dr. Jones began to experiment with this type of “spontaneous release by positioning.” His discovery led him to find that dysfunction generally exhibited itself through tender points, discrete areas of tenderness to palpation. As he found these points, he also began to develop treatment positions for them. His initial explorations were on the posterior surface of the body, but later he discovered the importance of treating points on the anterior body that related to those on the posterior surface.12 The principle of this style of treatment involves understanding the pattern of trauma, its dysfunctional stabilization, and its eventual resolution. The original trauma is described in the context of a segmental strain. This described scenario creates an overstretch of an agonist muscle and a reflexive contraction of the antagonist muscle. Immediately after the moment of strain, there is a recoil where the agonist muscle attempts to return to its original level of stretch. The speed at which this occurs, however, results in the reflexively contracted antagonist being unable to relax, resulting in a secondary persistent counterstrain of the antagonist muscle. The treatment for this problem involves shortening the antagonist to a point in which spontaneous relaxation occurs followed by a slow return to neutral, eliminating the dysfunction.13 The physiology of this treatment is thought to revolve around the activity of the muscle spindle fiber. This intrafusal proprioceptive fiber responds to relative length of muscle. In contrast

to the stretch receptors of the Golgi tendon organ, these muscle spindles seem to respond to increasing length by increasing tone as opposed to decrease. Muscle spindles are thought to be related to a reflexive protective mechanism and increasing the resistance to the muscle becoming overstretched. This is modulated by the gamma motoneuron, one of the types of neural fibers responsible for maintenance of muscle tone. By shortening these fibers during strain counterstrain treatment, this is thought to reduce the afferent stimulus to the spinal cord and subsequent down-regulation of the gamma efferent back to the muscle itself.14 Howell and colleagues demonstrated that osteopathic treatment with strain-counterstrain in Achilles tendinitis resulted in a reduction in stretch reflex amplitude but without changing H-reflex amplitude, suggesting a reset of the intrafusal mechanism without changing the spinal reflex.15 The principles of treatment are straightforward in their description, but again, the correct execution of this treatment is one that requires practice and patience on the part of the physician. The first step in treatment of dysfunction using strain counterstrain treatment is the identification of the “tender point.” This is usually a discrete, nonradiating area found within the belly of the muscle or at the muscular attachment at a body prominence. Multiple tender points may be found in a regionally related group of muscles and, in that case, the most tender point should be taken and treated first. These tender points are differentiated from myofascial trigger points in that there is not the characteristic radiation of pain that is typical of a trigger point.16 In order to quantify the amount of tenderness at the beginning of treatment, the patient is instructed that whatever tenderness is being elicited with palpation should be considered a 10/10 in intensity to begin. Next, the patient is positioned according to her comfort and the position is finely tuned until the pain is considered a 3 or less. Alternatively, the physician may initially suggest that the tenderness is worth one dollar, and query the patient as to when the tenderness is worth a quarter or less. This is the most unique aspect of any of the osteopathic treatments. As previously mentioned, osteopathic treatment is one that focuses on dysfunction and restoration of function and movement. Pain is considered to be a result of dysfunction and not treated per se. Counterstrain treatment is the only treatment in osteopathic manipulative medicine in which the level of tenderness is used as a guide to treatment and as an assessment as to the efficacy of the treatment after it is completed. While the position of greatest comfort is unique to every patient, there are general rules by which one can easily begin to see what positions will treat what problems. Texts on counterstrain are full with diagrams documenting treatment positions for tender points of all regions of the body, but all practitioners operate with the admonition to watch for “maverick” points that may not follow the typical patterns. Classically, points on the anterior aspect of the body respond to flexion where tender points on the posterior aspect respond more effectively to extension. Tender points that are lateral to the spine generally require some side-bending and rotation away from the tender point. Tender points along the posterior rib angles tend to be relieved by rotation and side-bending toward the side of the tender point with the addition of compression or distraction if the rib is in greater ease with exhalation or inhalation. Approaching the tender point is a step-wise process. Contact is maintained on the tender point with the palpating finger tip, preferably not the thumb to eliminate the practitioner’s appreciation of his own pulse. Additionally, the finger tips are more sensitive than the thumb to palpation. As the patient’s body position is adjusted to approximate the desired location, the patient is asked, “is this less

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tender?” If the answer is, “yes,” then a quantification of the improvement is obtained. If improvement is 70% or better, then that position is held for 90 seconds. If, however, the improvement is present but less than 70%, the position is fine-tuned to get closer to the point at which the counterstrained muscle fibers are shortened and afferent barrage from the muscle spindle subsides. When a position of comfort is obtained, the position is held for 90 seconds. This time length is optimal for allowing a neurologic reset of the gamma efferent barrage and releasing the underlying hypertonicity of the counterstrained muscle. At this time, the tender point continues to be monitored, but no pressure and no activity is taking place. The therapeutic action is based solely on the passive positioning of the patient and the time he or she is in that position. During the 90 seconds that the patient remains in that position, special attention should be given to the comfort of the physician and patient. The physician must hold the patient securely to allow for the patient to completely relax and facilitate the release of the tender point. For that to occur, the physician must be in a position that is supported and comfortable to limit fatigue of tonically held muscles and subsequent tensing of the patient because he or she no longer feels secure. After 90 seconds of positioning, the patient is slowly returned to the neutral position. This slow return is thought to minimize any secondary reflexive spasm of the treated tissue, re-initiating a tender point and dysfunction. The first 10 degrees of motion are the most crucial and should be accomplished very slowly, following those 10 degrees the return to neutral may be a little faster, but should remain smooth and gentle. Also important is the patient’s complete lack of effort in the return to neutral. At the beginning of the return, the patient is instructed: “I am going to bring you back to neutral and I don’t want you to help me at all. I want you to totally relax and let me do all the work.” This can be difficult for patients as they try to be helpful, particularly if they perceive that their weight is putting an undue strain on the physician’s body. It is incumbent on the physician to communicate firm control to the patient nonverbally by the amount of steady contact, grip, and smooth, controlled motion that the physician exhibits at this point in the treatment. When the patient is returned to neutral, the tender point is rechecked. At this time, the tenderness should be 70% improved or more. If improvement did not attain that level, then the treatment is repeated; the diagnosis is reevaluated; or the physician should look for another tender point, perhaps in a similar region, but also on the opposite side of the body, anterior or posterior. If suitable improvement is obtained, then other tender points can be treated, or the treatment session may be ended. As with other osteopathic treatments, the patient is instructed to limit daily activities to only those that are performed on a daily basis for the next 24 hours. This is to limit overuse while the neuromusculoskeletal system is integrating the effects of the treatment and accommodating to the relief of any biomechanical imbalance that may have been present as a result of the diagnosed dysfunction. Strain counterstrain treatment is an indirect technique. In contrast to muscle energy technique where the functional barrier is approached, an activating force is applied, and then the segment is moved through the barrier, this technique moves the segment away from its resistance into its ease. This movement away from the barrier, combined with 90 seconds of elapsed time, gives the neuromusculoskeletal system a chance to reset its aberrant firing pattern, and is an example of using an intrinsic activating force. This intrinsic force is usually breath or ease of positioning and allows for spontaneous correction. The advantage of using an indirect technique is

that the process of release is internally regulated and the potential to cause any harm to the patient through use of external force is minimized. This wide margin of safety and gentleness of technique allows for easy use in acute injury and when significant pain might be present. Therapeutic movements are generally slow in indirect techniques and the goal is generally toward palpable objective ease within the tissue. Treatment with strain counterstrain is specific toward alleviation of discomfort, making it even more attractive when applied to painful situations. The cervical spine region is unique because it articulates with the cranium superiorly and the thoracic cage inferiorly. Rotation, side-bending, flexion, and extension are all movements of the spine that are integral to the function of the cervical region and important to the organism. As the final common biomechanical pathway from the appendicular and axial skeleton toward the cranium, the cervical spine fulfills an important function for the organism, primarily by directing its sense organs—vision, hearing, smell, and taste—toward the external environment. Its remarkable freedom of movement provides a suspensory function during gait and a stabilizer to the cranium during rapid changes in directional movement. It serves to keep the gaze level and uses remarkable proprioceptive influences to sustain that during normal motion of the body. Closely associated with the cervical spine are the vertebral arteries and carotid arteries, which are crucial in creating the cerebral circulation. Venous drainage of the head through the jugular veins is through the region of the cervical spine. The two halves of the autonomic nervous system are in close proximity in the cervical spine with the cell bodies of the vagus nerve emerging from the jugular foramen of the cranium, providing parasympathetic function extending inferiorly from the brainstem to the level of C2 and the sympathetic cervical ganglia providing afferent stimulation to the head, neck, and cardiac regions. The viscera of the esophagus and trachea have their origins in the cervical spine. The importance of considering the anterior and posterior musculature in stabilization of a particular region is easiest to appreciate in the cervical spine. Posteriorly, the erector spinae group of muscles along with the upper splenius capitis and cervicis muscles interface at the cranial base with the rectus capitis muscles along with the obliquus capitis muscles. Anteriorly, the sternocleidomastoid provides a significant support against rapid extension of the head on the cervical spine, and longus colli and capitis provide support and aid in flexion of the neck. The uppermost two cervical vertebrae are the atlas and axis, both of which are considered atypical cervical vertebrae. The axis, C1, articulates with the cranial base and C2. It lacks a vertebral body or transverse processes. The articulation with the occiput is primarily designed to allow for flexion and extension of the head on the cervical spine, whereas the articulation between C1 and C2 allows for the primary rotation of the head to the right and left. This is because the atlas and axis behave as one segment providing two distinct motion functions. The contact between C1 and C2, the dens and its surrounding ligaments and cartilage is actually a modification of a vertebral body and intervertebral disk. The remaining cervical vertebrae from C3 to C7 are the typical vertebrae with a round vertebral body and intervertebral disc. Unique to these vertebrae are their nearly horizontal articular facets in the superior segments that become progressively more oblique in their presentation as they move inferiorly, but still oriented in an anterior to posterior plane. Additionally, the transverse processes of the cervical vertebrae from C2 to C7 have foramen that allow the passage of the vertebral arteries bilaterally and vertically. These converge over the atlas and enter the foramen magnum where they produce the posterior arch of the circle of Willis at the brainstem.8

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Because of the anatomy of the articulations within the cervical spine, the dysfunctions tend to occur with rotation and side-bending to the same side. This may or may not occur with an accompanying flexion or extension component because the neutral position of the cervical spine tends to rest in extension with a cervical lordosis. As a result of this neutral extension, any dysfunction that is found and diagnosed with rotation and side-bending to opposite sides is thought to be a result of significant trauma that has created a constellation of forces that impose nonphysiologic motion and function. When electing to use strain counterstrain, scanning not only includes motion testing but also palpation for tender points in the region where dysfunction has been identified. Again, this necessary palpation for tenderness is a unique feature of preparation of treatment with counterstrain. Identification of tender points can be approached by two methods. In one, a previous knowledge of the typical locations of tender points in the region are known and the practitioner scans for likely locations in the region of the dysfunctional segment. In another, palpable change in the tissue tension, such as ropiness, bogginess, or bands are palpated, the specific tender point is localized, and then the practitioner uses that information to further focus the scan and segmentally define a dysfunction. In either method, identification of a tender point is an extension of, or palpatory evidence of, segmental somatic dysfunction. Importantly, it is not sufficient to simply find a tender point without further investigation as to the defining characteristics of the dysfunction, tempting though it might be. Treatment positions for tender points in the cervical spine fall into three broad categories. Specific exceptions to these generalizations occur but are beyond the focus of this chapter and necessitate further study. Typically, the two types of tender points are posterior and anterior. The posterior points fall directly over the spinous processes of the cervical spine and generally require passive extension as a position of comfort. An alternative location for the posterior points is just on the lateral and inferior edge of the spinous process (Fig. 18-4). Treatment of these points requires extension, sidebending, and rotation away from the side of the tender point for resolution. The anterior tender points are found along the anterior surface of the transverse processes of the cervical spine and require side-bending toward and rotation away from the side of the tender point combined with flexion of the cervical spine to obtain resolution of the tender point (Fig. 18-5).14 Specifically, in the subsequent examples, the positions for treatment of posterior C2 (PC2), posterior lateral C3 (PLC3), and

anterior C5 (AC5) are shown. For each of these positions, the ­previous principles of treatment apply: (1) identify the tender point; (2) find a position of at least 30% improvement; (3) hold the position 90 seconds; (4) slowly return the patient to a neutral position; and (5) recheck the tender point for resolution.

Figure 18-4  Positioning for treatment of posterior C2 on the right (PC1).

Figure 18-5  Positioning for treatment of anterior C5 tender point (AC5).

High Velocity Low Amplitude: Thoracic Spine High velocity low amplitude (HVLA) is a direct technique in which a segment or joint is brought to its restrictive barrier and a short thrust is applied, forcing the segment or joint through the barrier and resolving the dysfunction. This style of manipulation is usually the most recognizable form of manual medicine because it is the most dramatic. This is typically what a patient incorrectly describes when she says, “The doctor cracked my back.” The diagnosis that precedes this treatment is commonly described as “my back being out.” Each of these colloquialisms is inaccurate, in part, and presents misconceptions and oversimplifications, but describes an easily recognizable and memorable treatment experience. HVLA was the dominant form of osteopathic manipulation taught in the United States for the first half of the 20th century until the advent of muscle energy treatment. Interestingly, although this was so widely taught in the early days of osteopathy, this treatment was probably not what Dr. Still practiced. Through limited descriptions of his treatments in his writings and one short film clip that shows him treating a shoulder, along with writings of some of his students, Still probably did not treat with HVLA, but more likely treated from the myofascial and articulatory perspective, some of which will be described later in this chapter. Dr. Ray English wrote of Dr. Still’s technique “I have seen [Dr. Still] adjust lesions but I have never heard him adjust a lesion.”17 It is reported that D.D. Palmer, the founder of chiropractic in 1895, visited Dr. Still in 1893, was treated by him, and had numerous meetings with him. After the “discovery” of chiropractic, “the Palmer method” was demonstrated by Dr. C.E. Achorn at the American Osteopathic Association convention in 1900. Although this was described as “a very crude and very poor imitation of the kind of manipulative therapy Dr. Still practiced,4” it is thought that Palmer’s influence may have been reabsorbed into the osteopathic profession and elaborated as osteopathic HVLA treatment. The ease of the description of this treatment seems to belie its pervasiveness as the dominant style of treatment taught in the osteopathic colleges until newer methods were developed—eventually leading to the elaboration of Still Technique5 (a more developed description of some of the articulatory

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techniques thought to represent Still’s original style) in the 1990s. Because of its universality of application and simplicity of execution, HVLA continues to be the most popular style of manipulation in osteopathic practice.18 The skill of execution of HVLA technique lies in the localization of the barrier and the quality of the thrust. In HVLA, the barrier is palpated by movement of regional treatment zones, typically in opposite directions in an effort to “lock out” the barrier. In the axial spine, the zygapophyseal joints are those that are most commonly treated with HVLA. Generally, the anatomy of those joints and their direction of articulation define the motion that is undertaken by the physician to engage the barrier and later, the application of thrust. The name, “high velocity low amplitude”, is an apt descriptor for the type of force applied. Classically, a short 1 ⁄8-inch thrust is quickly applied to the barrier and then the region is rechecked. This can be a difficult concept for a beginning student to grasp. This thrust quickly moves the articulations apart and often results in an audible pop or crack. No definitive explanation for the therapeutic benefit of this procedure has been agreed on, although neural mechanisms along with alteration in cross-link connective tissue adhesions has been proposed.5 This technique is particularly indicated for dysfunctions of a chronic nature in otherwise healthy adolescents or adults. Of all manipulative medicine techniques, those of the high velocity style are fraught with the highest morbidity. Of the regions that can be treated with high velocity manipulation, the cervical spine carries with it the highest morbidity and potential mortality. The American Osteopathic Association published a position paper in 2004 after reviewing the reported adverse events associated with cervical HVLA treatment as well as its benefits and concluded that osteopathic manipulative treatment of the cervical spine with HVLA treatment is effective for neck pain and is relatively safe, especially in comparison to other common treatments.19 Because of these risks, relative contraindications to use of HVLA procedures include rheumatoid arthritis, Down’s syndrome, bony carcinoma, osteoporosis, and osteomyelitis. The benefit of the application of this technique, in skilled hands, generally outweighs the risk in most situations and provides rapid relief of dysfunction and allows for great patient satisfaction.

Thoracic Spine The thoracic spine consists of twelve thoracic vertebrae and creates a biomechanical transition between the cervical spine and the lumbar spine. This transition is reflected in the anatomic and functional differences as the thoracic spine changes along its length (See Fig. 18-1). The spinous processes of the first three thoracic vertebrae closely resemble those of the cervical vertebrae, generally pointing directly posterior; however, these spinous processes tend to point slightly inferior. The next three thoracic vertebral spinous processes point slightly more inferior and end in the horizontal plane of the intervertebral discs of T3-6. This trend continues in the next three thoracic vertebrae until the spinous processes end at the vertebral body of the segment inferior to the one above. T10-12 represent a functional transition toward a more lumbar appearance and reverses the anatomic trend of the first nine vertebrae as the spinous process ends at the horizontal plane of the segment of its origin.11 Similarly, the thoracic spine has a unique anatomy of its articular facets, transitioning from a superior-inferior orientation with an oblique orientation posterior and inferior, similar to the

cervical segments in the upper thoracic region, to a more mediallateral orientation in the lower thoracic region, similar to the lumbar segments. The orientation of these facets has a direct affect on the angle of thrust when performing osteopathic manipulative therapy (OMT) on the thoracic spine. Closely associated with the thoracic spine are the nerve roots that emerge from the neural foramina created by each pair of thoracic vertebrae. Immediately adjacent to these neural elements are the thoracic chain ganglia, representing the thoracic segment of the sympathetic nervous system. Importantly, the cell bodies for the preganglionic fibers occur at the segments T1-L2. Addressing dysfunction within these segments provides a useful approach to the potential impact of imbalance within the autonomic segments and visceral disease. I.M. Korr, PhD, an early neurophysiologist within the osteopathic profession, proposed the model that irritation and facilitation within the autonomic nervous system was the first predisposing factor to illness that could be expressed in the body.5 This facilitation and subsequent elevation in sympathetic nervous system tone with its tendency toward vasoconstriction created an environment that would be limited in its capacity to support health by a restriction in vascular flow. This is one of the primary aspects of an osteopathic physiology of pathogenesis. This is known as the somatovisceral reflex. Because visceral afferents synapse on cell bodies within the spinal cord that are closely associated with somatic spinal afferents that then converge on somatic spinal efferent nerves, irritation within the viscera can reflexively exhibit spinal muscle hypertonicity that may be palpable as tissue change and somatic dysfunction. This can provide meaningful clues from a structural examination toward the presence of visceral illness. This is known as the viscerosomatic reflex. Because of the preponderance of autonomic cell bodies in the thoracic spine, this region is often used as a method of approach toward visceral illness from an osteopathic perspective. By releasing somatic dysfunction in any region of the thoracic spine that is dysfunctional, the opportunity for normalization of the autonomic nervous system is hypothesized to occur. Reducing sympathetic tone sets the stage for the restoration of health by improving vascular and interstitial fluid motion. Diagnosis of thoracic dysfunction is made using the screen, scan, and segmental definition methods previously described. Alternatively, the thoracic spine may be defined in the following manner. After screening determines that a dysfunction is present in the thoracic region, palpatory scanning in the seated position identifies tissue texture changes characteristic of dysfunction (i.e., segmental tissue change associated with a rotation of the transverse process to the right or left). This feels like a prominence in the paravertebral tissue that is firmer than simple muscle tension—an asymmetrical prominent bony landmark in the tissue of that particular segment. The level of dysfunction is identified by counting spinous processes, keeping in mind the variations in the thoracic levels relative to the spinous processes characteristic of this region of the spine. When these changes are localized, thumbs are placed on the region of the transverse processes and the patient is asked to bend forward. As the patient bends forward, the palpating hands identify any changes in position or motion at the rotated transverse processes. If the asymmetry improves in the flexed position, the position of ease is identified as “flexed.” If the asymmetry does not improve, the patient is asked to sit up straight and arch his or her back slightly with the neck slightly extended, causing thoracic extension. If improvement in the asymmetry of the transverse processes is identified, the position

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of ease is identified as “extended.” If no change is palpated in either position, flexed or extended, then the position of ease is identified as “neutral.” Because of the principles of spinal mechanics known as Fryette’s Laws,20 a dysfunction that is either flexed or extended also exhibits rotation and side-bending to the same side and a dysfunction that is neutral exhibits side-bending and rotation to opposite sides. In this example, if T5 was found to exhibit rotation to the right and found to be in ease with flexion, it would be identified as “flexed, rotated right, and side-bent right.” If it was found to be in ease with extension, it would be identified as “extended, rotated right, and side-bent right.” If no change was palpated with flexion or extension, it would be identified as “neutral, side-bent left, rotated right.”

Thoracic HVLA Treatment 1: Flexed Dysfunction As a direct technique, HVLA demands segmental definition diagnosis of somatic dysfunction so an appropriate position into the restrictive barrier can be introduced before thrusting. In this technique, the patient is placed in the prone position and the diagnosed segment is identified. The physician stands to the side of the patient that exhibits thoracic rotation dysfunction and places his hands on the thoracic region with hypothenar eminences on opposite sides of the diagnosed segment (Fig. 18-6). The hands are placed in opposite directions so that the fingers are pointing cephalad on the side of the thoracic side-bending and caudad on the side opposite the side of thoracic side-bending. For example, in the diagnosis of “T5 flexed, rotated, and side-bent right,” the physician stands on the right side of the prone patient and places the hypothenar eminences on the region of the transverse processes with the fingers on the left side of the spine pointing cephalad and those on the right side pointing caudad. This provides a position for creating tissue tension that encourages leftward side-bending. The tissue tension and motion restriction is tested in that position, moving the tissue into the barrier by slightly increasing the side-bending to the left through opposite motions of the cephalad and caudad hands. The patient is instructed to take a deep breath and exhale. Contact with the tissue is maintained through inspiration and followed through exhalation as the barrier is more significantly engaged through slightly greater increases in pressure. At the end of exhalation, the barrier is completely engaged and a slight 1⁄8-inch thrust toward the table and with

Figure 18-6  Prone cross-arm HVLA treatment for mid-thoracic dysfunction.

both cephalad and caudad pointing hands quickly moving in opposite directions, in a twisting manner.

Thoracic Treatment 2: Extended Dysfunction Treatment of this type of dysfunction is performed with the patient in the supine position. A diagnosis is made of the dysfunctional thoracic segment. For this example, the diagnosis is T5 extended, rotated, and side-bent right. The physician stands on the side of the supine patient that is opposite that of the rotation. In this example, the physician would stand on the left side of the supine patient. The patient is asked to cross both arms across the chest snugly and grasp the shoulders. This provides the elbows as a point of contact for the physician’s sternum, draws the scapulae laterally for better contact with the thoracic spine, and tightens the fascia of the thoracic cage, allowing for a more specific direction of force into the segmental barrier. The cervical-occipital junction is supported with the right hand of the physician, whereas the left hand reaches around and behind the patient to make contact with the dysfunctional thoracic segment. An open-handed fist is used to localize the dysfunctional segment by making contact with the thenar eminence on the rotated transverse process (Fig. 18-7). The patient’s torso is brought anterior into flexion and then relaxed over the open-fist fulcrum balance force between the physician’s sternum, the fulcrum, and the supporting hand on the occipitalcervical junction. When forces are balanced and the barrier is engaged, the patient is asked to inhale and exhale. On the exhaling breath, the physician follows the thoracic cage as it collapses in anterior-posterior diameter and at the end of exhalation, applies a short 1⁄8-inch thrust through the sternum, patient’s elbows, and through the dysfunctional articulation. The direction of this thrust has a slightly cephalad orientation as the motion is intended to create a relative flexion of the thoracic segments that are restricted in extension (Fig. 18-8). Two significant points of refinement in the successful approach to HVLA in clinical practice are accuracy of engagement of the functional barrier and appropriate application of force. The application of force is sometimes described as that amount of force necessary to squash a grape under one finger without sullying your

Figure 18-7  Correct placement of thenar eminence on posterior transverse process in preparation for supine HVLA.

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Figure 18-8  Positioning for supine HVLA technique in the thoracic region.

finger with the juice. This is an excellent image of the accuracy, the speed, the type of force, and the slight recoil that occurs in a thrust technique. There is no wind-up and no follow-through. This is a specific and directed application of rapid compression intended only to move the intended segment past the barrier and no more. This force may be accompanied by a sound of pop or click but this is not necessary for the treatment to be effective. Effectiveness of treatment is measured by reevaluation of the diagnosed segment after the treatment is performed. Localization of the barrier is essential to the appropriate execution of the thrust in HVLA. These treatments often use regional leverage as a way to minimize the amount of overall force applied to a given segment. For example, in the supine application of HVLA to the thoracic spine in the example just mentioned, rotation, sidebending, and the balance of flexion and extension are maximized to localize all forces exactly at the segmental articulations that are dysfunctional. Too much of any of these motions will disturb the focus of applied force either localizing it to an unintended segment or diffusing the force too broadly across multiple segments resulting in an ineffective thrust. High velocity, low amplitude osteopathic manipulation can be a rapid and effective approach to dysfunction of the thoracic region but can also be applied to any dysfunctional region of the body. Further training allows for discovery of different positions to treat dysfunction of different regions, but the principles of treatment will remain the same. This treatment requires specificity of application of force to be effective and any variation from that specificity increases the likelihood that the treatment will not be effective or potentially harmful.

Myofascial Release: The Extremities The origin of myofascial release technique in osteopathy dates to the time of A. T. Still. In Principles of Osteopathy he writes: “we think we prove conception, growth, and cause of all diseases to be in the fascia.”3 Given the importance that he attaches to the fascia, it is likely that within his style of technique, treatment of the fascia was given significant consideration. Considering the ubiquity of fascia within the body it is easy to overemphasize or casually ignore its presence. Treatment of the fascia can be superficial or deep and

may be applied from a perspective of direct or indirect technique or a combination of the two. Conventional anatomic approaches to fascia tend to overlook its presence as an obstruction to the study of more exciting tissue, muscles, nerves, vessels, glands, bones, and viscera. The very extent of its presence in the human body belies its importance. Embryologically, this connective tissue network provides the matrix for all of the differentiated organs and tissue to develop and so provides support and guidance as these tissues form. Following ontogenetic development, the fascia supports the entire structure of the human organism and extends its influence from the loose connective subdermal connective tissue inward through muscle septa, perineural tissue, perivascular support, forming visceral and parietal peritoneum, and extending its influence even further to the interstitial connective tissue network between cells. Because of its universal influence, fascia is said to be both continuous and contiguous throughout the whole body. It provides a matrix for the interstitial fluids and the extracellular aspects of the immune system. Functional freedom within the fascial network is essential to the proper functioning of all aspects of the human organism. Although it is true that this connective tissue network is necessarily influenced by any manipulative technique because of its universal presence, specific myofascial release technique is different in its focused palpatory attention to that tissue. Treatment can be focal such as a superficial connective tissue release over the knee by articulating the relative torsional motion at the fascia of the femur and tibia, or it can be remarkably remote such as treatment of the upper extremity as a long lever in relation to the thoracolumbar fascia and its influence on the pelvis and lower extremity. The diversity of approaches is akin to the phenomena of smoothing out a wrinkle in a tablecloth. One can choose to address the wrinkle directly, smoothing it out with one’s hands; alternatively, one can choose to stand at the end of the table and tug along the length of the cloth until the tension reaches the region of buckling and the slack is balanced again. Most conventional approaches to fascia and naming of fascia create artificial distinctions between types and locations of fascia: Scarpa fascia, Colles fascia, Buck fascia, Sibson fascia, and so on. The naming of fascia in this manner detracts from its interconnectedness when, in an example of functional anatomic reality, the distinction between the fascia of the humeral and radioulnar joint is indistinguishable in its continuation as the fascia of the biceps and brachialis muscles. Treatment with myofascial release technique becomes first a matter of perspective on the totality of the connective tissue network with its presence and functional importance everywhere in the body. Myofascial technique often makes use of motion stacking when addressing dysfunctioning from the position of the extremities. Motion stacking occurs when one part of the extremity is moved into a chosen position according to one’s intention and then begins to move another portion of the extremity into another position with the intention of holding the first position. For example, in addressing the upper extremity from a distal to proximal approach using direct fascial technique, first the hand and wrist is moved into a position that engages resistance in as many fascial planes as possible. Next, while maintaining that position with the wrist, the forearm is secondarily engaged in resistance in as many fascial planes as possible. This process is continued proximally along the upper extremity until the motions are stacked into the axilla or proximally. At that point, the phenomena of hysteresis or creep occurs and the fascia will release spontaneously while held in tension. Attention to

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the different regions of an extremity can be engaged separately also, by first treating the wrist, returning to neutral, treating the forearm, returning to neutral, and so on.

Palpation Exercise As an introduction to the fascial concept, this exercise in palpation can help to hone one’s palpatory focus to the relative tensions or looseness in the fascia. Start with your patient in the supine position standing at the patient’s right side, just caudad to the wrist. Pick up the wrist and slowly maintain some light tension through the arm and shoulder. Your attention should be tuned to the tension in the connective tissue with the intention of palpating the different levels of tension throughout the different levels of the extremity. Next, turn the wrist into pronation slowly until you feel the engagement of the humerus. Continue to internally rotate the humerus until you begin to feel and endpoint of the connective tissue near the glenohumeral region. When you have found that endpoint, ask your patient to turn his or her head to the right slowly. Observe the changes in tension that occur along the upper extremity during the rotation and after, when at rest in right cervical rotation. After a moment, ask the patient to turn his or her head to the left slowly and feel the differences in tension that occur as there is movement through that rotational arc. Ask the patient to bring the neck into a neutral position again, and again maintain your tension in the upper extremity. When you have regained your palpatory focus, have the patient inhale deeply and hold the breath for a moment. Feel for any changes in the upper extremity with that phase of respiration. Have the patient relax in breathing for a few moments and then, while you maintain your tension, have him or her to inhale deeply, exhale, and hold the exhale for a few moments. Feel for any differences in the tension pattern of the upper extremity while the patient is in that phase of respiration. This exercise begins to increase an awareness of the palpation necessary to perform myofascial release along with an appreciation of the interrelationship of motion at disparate areas of the body and an appreciation of the influence of respiration on the fascial network.

The Extremities The upper and lower extremities in the human body occur as appendicular extensions of the thoracic cage and of the abdominal cavity, embryologically.21 The human extremities provide us with locomotion to find sustenance and with methods of connecting with the world from our hearts and touching the solid forms around us. Anatomically, they consist of one long bone that articulates with the axial skeleton through a highly mobile “ball and socket” type of joint, a double-bone that articulates with the first via a hinge joint, with the upper extremity example of this being able to fully supinate and pronate, and finally a distal multiply articular appendage designed for locomotion or object manipulation and kinesthetic awareness ending in five distal phalanges. For the purposes of the elaboration of myofascial technique, each of these extremities can be addressed individually in treatment of the extremity itself, or it can be viewed as a long lever that, when activated, can be used to affect the integrity of the fascial network at regions significantly distal to the point of motion input. The connective tissue fascial network of the extremities begins in the superficial layer as loose connective tissue, or areolar connective tissue, occurring subdermally and often including a panicular

layer of adipose tissue. Internal and contiguous to that layer is the intermediate layer of connective tissue that represents the fascia surrounding the muscle layers. This layer of fascia invests into the muscle tissue itself dividing the muscle into individual fascicles and then providing intercellular support. This intermediate layer continues centrally until it becomes a deep fascial layer that integrates into the ligamentous and periosteal tissue of the upper extremity. This fascia begins proximally as the investing fascia of the axial skeleton, nervous system, and mediastinum, extending radially through the viscera out to the visceral pleura, parietal pleura, thoracic cage, and the superficial muscles of the anterior and posterior thorax and distally to the proximal anterior and posterior shoulder region. Inferiorly, this fascia begins axially, investing in the retroperitoneal structures and viscera, the abdominal viscera, mesenteries, visceral peritoneum, parietal peritoneum, extending out through the superficial musculature of the anterior and posterior abdomen, extending into the pelvis and distal to the myofascial network of the girdle of the hip.22 This litany of structures is only a rudimentary description of the totality of the presence of the fascia within the human organism and could be elaborated in much greater detail.

Myofascial Release Assessment and diagnosis of the extremities is similar to the axial spine in that identification of tissue texture change and restriction in motion are identified and the identified joint motion is named in its motion of ease. The preponderance of dysfunctions in the upper and lower extremity occurs not in the major motions of the joint but in the secondary, often involuntary, motions. These are often gliding or translatory motions that provide an important adaptive role but are generally not under direct voluntary control of the musculature. For example elbow pain can be traced, many times, to a restriction in the medial and lateral translatory glide that is present at the humeral and ulnar joint. This must be tested passively by the physician for a structural diagnosis to be obtained. With the significant number of joints that may possibly be dysfunctional in each of the extremities, a detailed description for testing will not be discussed here but is instead a subject for further study. Upper Extremity In this example, treatment of the upper extremity begins with the patient in the lateral recumbent position with the extremity to be treated, off the table. Treatment begins proximally by engaging the fascial tissue surrounding the scapula. The physician’s hand surrounds the posterior portion of the scapula and passively moves it cephalad, caudad, medial, and lateral. When a barrier is reached, the tissue is permitted to release spontaneously or with respiratory assistance as in the palpatory exercise example. Next, the deep fascia of the extremity is addressed by abducting the arm while the fascia of the anterior axilla and then the posterior axilla is stabilized. The fascia of the elbow is next addressed by stabilizing the elbow while slowing supination and then pronating the forearm to the endpoints of motion in each direction. The fascia of the wrist is addressed through slow articular stretching of the radiocarpal joint; the metacarpals are individually articulated with attention to the connective tissue; and the fascia of the phalanges is mobilized as well. Finally, the entire upper extremity is brought into abduction and external rotation, engaging the pectoralis fascia along with the myofascial network of the upper extremity. Next internal rotation and adduction of the upper extremity is performed, engaging the myofascial tissue of the upper extremity along with the posterior

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Figure 18-9  Upper extremity fascial release opening axillary fascia.

trapezius, latissimus dorsi, and other axial fascial connections, superficial and deep (Fig. 18-9). The Lower Extremity Treatment of the lower extremity with myofascial release technique begins by placing the patient in the supine position. This treatment technique makes use of the joints of the lower extremity as anchors for the fascial components of the interarticular soft tissue and the connection of the lower extremity to the pelvis as it engages the myofascial connections in the pelvis, abdomen, and axial skeleton. With the patient in the supine position, one leg is flexed creating an equilateral triangle with the distance between the femur, tibia, and the space between the hip and foot on the table being roughly equivalent. The foot is internally rotated to its fascial barrier, and the caudad hand is placed over the tibial-talar region to stabilize the internal rotation. The cephalad hand is placed on the knee and by moving the knee in a medial direction, the hip is internally rotated to its fascial endpoint. This endpoint is held while the patient is asked to inhale deeply, exhale, and hold the exhale as long as possible. At the end of the exhale, typically just before the patient takes the next breath, the tissue will relax and a new fascial barrier will be reached. This can be repeated until a maximum amount of motion is obtained through the lower extremity fascia. The lower extremity is then returned to the neutral position and the foot is taken out of internal rotation and placed in the neutral position. Next, the foot is externally rotated to its fascial barrier and held with the caudad hand over the tibial talar region. The cephalad hand is now placed on the medial aspect of the flexed knee and the hip is externally rotated to its fascial barrier, the patient is asked to inhale deeply and hold the inhalation until unable to hold it any longer. Again, at the point of exhalation, the tissue will relax and a new fascial barrier is reached. This treatment is repeated until no further release is appreciated. The lower extremity is then returned to a neutral position and the identified dysfunction is rechecked for resolution. This treatment efficiently addresses dysfunction at multiple levels of the lower extremity and engages the fascia of the anterior and posterior pelvis. Internal rotation of the lower extremity with the knee in flexion and the ankle stabilized creates a relative inversion of the talocalcaneal joint, internal rotation of the tibia,

Figure 18-10  Lower extremity fascial release position.

posterior lateral glide of the tibia at the femur, posterior glide of the proximal fibula, internal rotation of the femur at the acetabulum, and associated fascial engagement of the posterior pelvis including the gluteal and piriformis regions. Internal rotation of the lower extremity largely creates the opposite motions and tensional engagement of the anterior pelvis and internal rotators of the hip including the anterior fibers of the gluteus medius and minimus, the adductor longus and brevis, the pectineus, the medial hamstrings (semitendinosus and semimembranosus) and the tensor fascia latae (Fig. 18-10). Myofascial technique can be applied to any area of the body effectively with focused palpation and knowledge of the musculoskeletal anatomy. Although both treatment techniques described here are direct techniques, application of indirect myofascial technique methods is also appropriate by combining palpation and regional motion to find the greatest ease or path of least resistance as the dysfunctional region is moved away from the barrier and an allowance of spontaneous resolution through intrinsic movement toward health and functional homeostasis occurs.

Osteopathy in the Cranial Field Treatment of the cranium fundamentally applies the principles of osteopathic manipulative treatment for the rest of the body, but involves a greater sensitivity to palpatory cues and appreciation of the subtle motion in the region of the head. Central to the practice of osteopathy in the cranial field is the understanding of the mechanics of the cranium and how that motion is reflected in the rest of the body. A respect for the potentially negative impact of treatment of the cranial region is also necessary and extensive treatment should not be undertaken by the beginner, but should only be attempted after sufficient introductory training by an instructor-led course. To that end, this chapter will cover only principles of cranial technique with an example of treatment that is effective and safe to apply by relatively inexperienced hands.

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The origin of cranial osteopathy as an extension of other types of osteopathic manipulative treatment is credited to William G. Sutherland, DO, a student of Dr. Still. The moment of its origination was when young Dr. Sutherland, walked past a model of a disarticulated skull in 1899 at the American School of Osteopathy, and “like a blinding flash of light came the thought—beveled like the gills of a fish and indicating articular mobility for a respiratory mechanism.”23 This began his study and development of cranial osteopathy. He later wrote that he was merely following Dr. Still’s advice to dig on as Dr. Still earlier wrote, “the cerebrospinal fluid is the highest known element that is contained in the human body, and unless the brain furnishes the fluid in abundance a disabled condition of the body will remain,” and mandated that, “this great river of life must be tapped and the withering field irrigated at once, or the harvest of health be forever lost.”3 Dr. Sutherland devised mechanisms to create dysfunction in his own cranium, studied the effects it would have, and then developed treatments to resolve them. He wrote The Cranial Bowl in 1939 and taught the cranial concept to interested physicians from 1940 to 1953.24 The cranial concept was a development of the mechanical principles of the cranial motion combined with the motion of the cerebrospinal fluid and the relationship of both to respiration. The combination of all three of these aspects he combined as the primary respiratory mechanism. Dr. Sutherland elucidated five fundamental principles of the cranial concept: (1) the fluctuation of the cerebrospinal fluid, (2) the function of the reciprocal tension membrane, (3) the motility of the neural tube, (4) the articular mobility of the cranial bones, and (5) the involuntary mobility of the sacrum between the ilia. Fundamentally, this concept states that primary respiration, the fundamental metabolic cellular process of existence, is driven first intrinsically through the related components of the central nervous system including the cerebrospinal fluid. Although each aspect of the components of the primary respiratory mechanism have been studied in anatomic and physiologic detail,25 this overriding concept of the function of the primary respiratory mechanism remains elusive and falls somewhere between the domains of physiology and phenomenologic epistemology. While detailed explanations about the palpatory diagnostic findings are well beyond the purposes of this chapter, a cursory illustration of some of the aspects of this concept will be attempted here. The bones of the cranium develop embryologically as either membranous bone or cartilaginous bone depending on their location. In general, the bones of the base of the cranium, the basiocciput and the sphenoid and petrous temporal arise out of cartilage, whereas the temporal squamous, occipital squamous, parietal, early frontal bones arise out of membrane. These slowly approximate each other as development continues after birth until they interdigitate during late ossification and become sutures. These sutures are not fused, but are largely patent with dissectible connective tissue fibers, lymphatics, and occasional nerve fibers present. The patency of the sutures allows for motion and this has been recorded and documented. The motion that occurs at these sutures is reflective of a deeper motion that drives them, and the development of the articulations is a result of that motion. With fine palpation, it is possible to appreciate a subtle cyclical expansion and contraction of the cranium with a rate of 6 to 12 oscillations per minute and with a variable amplitude.26 This motion is first appreciated as a flexion and extension that occurs at the cranial base in the synchondrosis of the sphenoid and base of the occiput. Motion is distributed to the paired cranial bones of the temporal and parietal that articulate the

cranial base, and flexion and extension then becomes internal and external rotation. This combination of motions—flexion, extension, internal and external rotation—translates into a palpatory experience of a rhythmic expansion and contraction of the cranium. This motion is intrinsic and primary, but is also associated with respiration and extends its influence to all the tissues of the body as inspiration is linked with external rotation of all the paired bones of the body and exhalation is linked with internal rotation of all the paired bones of the body. Diagnosis of the cranial region involves a detailed appreciation of the motion of the primary respiratory mechanism including the different movements of the cranial bones and appreciation of the ways in which they can become dysfunctional. As in any other joint of the body, certain common patterns exist and are readily palpated by trained hands. Treatment of the cranial region follows principles that apply to osteopathic treatment of the rest of the body, namely treatments that are direct or indirect in their approach. Direct treatments gently engage the functional barriers to motion of the cranial bones and use respiration or voluntary muscular contraction, including respiration, as activating forces to restore normal function. Indirect treatments move the affected portion of the cranium away from the barrier and allow for intrinsic homeostatic balancing mechanisms, including respiration, to allow for spontaneous correction and restoration of normal function. Again, because the cranium is the home to the brain and brainstem, this action must be performed carefully and with great respect for the impact that treatment can have, not only on the cranium but also on the functioning of the entire organism.

Palpation Exercise If one is to appreciate the palpatory experience of osteopathic treatment within the cranial field, the following exercise is presented. Treatment of the cranium is usually applied with the patient in the supine position. The physician sits at the head of the table on a chair that is at a height such that the elbows can rest comfortably without disturbing the erect seated posture of the practitioner. One of Dr. Sutherland’s students, Rollin E. Becker, DO wrote about establishing a treating fulcrum in a region other than the hands to allow for the greatest palpatory sensitivity.27 This fulcrum is usually the forearm or elbow and this portion of the upper extremity makes firm contact with the treatment table to allow for less distracting proprioceptive input in the hands and fingers. The hands are lightly placed on the vault of the cranium, thumbs touching and off the cranium to prevent over compression (Fig. 18-11). The index finger rests in the region of the greater wing of the sphenoid posterior to the lateral canthus of the eye. The middle finger rests just superior to the auricle. The fourth digit rests just inferior to the auricle and the fifth digit is posterior and inferior to the mastoid process in the region of the squamous portion of the occiput. When this position is achieved, the physician must take account of the amount of pressure that he is imposing on his patient. The amount of pressure must be enough to make light contact, but no more, because undue pressure can negatively affect the quality of the intrinsic motion present within the cranial vault. The physician checks his posture and relaxes as much as possible, again to reduce the amount of extraneous proprioceptive input, allowing for the greatest sensitivity to subtle motion. Next, the physician focuses on the space occupied between his palpating hands rather than what is happening at the surface under his fingers. Focusing on that space allows for the appreciation of the rhythmic alteration of the shape of the volume

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Figure 18-11  Vault hold.

Figure 18-12  Hand position for suboccipital release.

under his palpating hands. Commonly, he might first appreciate the rhythmic oscillations of respiration as it is transmitted up to the cranium or the cardiac pulse as it resonates into the cranium, but the cranial rhythm is a movement that is independent from that. With continued practice and refocus it is possible to palpate the cranial rhythm with its 6 to 12 cycles per minute periodicity and variable amplitude. This is the starting point for appreciation of the normal functional movement of the cranium, all cranial diagnosis, and subsequent intervention or treatment.

suboccipital tissue, allowing a normal relaxation as the pressure is increased. Importantly, only enough pressure necessary to engage the tissue is needed here (Fig. 18-12). Too much pressure can cause undue discomfort for the patient and becomes fatiguing to the hands of a new practitioner. Too little pressure and the technique is simply ineffective. Once the initial release of positioning is obtained, the practitioner can appreciate an asymmetry of tension within the tissue. Increasing the pressure on the side that is less tight, attempting to balance the tension between the two sides allows for a release of the tissue on the more restricted side. This is an indirect approach as we are moving into the ease of the tissue and allowing for a spontaneous correction. This anteriorly directed contact in the suboccipital region continues until no further release of the tissue is appreciated by the practitioner, usually within a few minutes. To fully appreciate the effect of this procedure, the fingers of the treating hands increase in their extension, supporting the suboccipital region by themselves with little support from the palms of the hands. This approximates the extension at the cranial base that Dr. Still experienced with his nap on the plough rope. When completed the patient is slowly returned to neutral and the tension of the tissue at the base of the cranium is rechecked. This simple treatment can have dramatic impact on diverse regions of the body, from the neurocranium and viscerocranium, to the thoracic and abdominal viscera, to general responses to pain along with other functional medical problems.

Treatment: Release of the Cranial Base and Atlas One of the significant portions of cranial anatomy is reflected in the articulation between the base of the occiput and the atlas. This area is rich with neural, vascular, and fascial structures. The base of the occiput near the atlas is the location of the jugular venous foramen in the articulation between the occiput and the temporal bone. This foramen provides venous drainage from the cranial vault along with the exit of cranial nerves IX, X, and XI. In addition, the cell bodies of the vagal nucleus descend in the upper spinal cord to the level of C2. At the cranial base, the dura still has some freedom of motion before it becomes attached at C2. A small fascial connection between the suboccipital muscles called the nuchal ligament is found in this region also.28 This is the final common pathway for all forces rising from the lower extremities, trunk, and upper extremities as the transition is made from the relatively mobile spine to the relatively immobile cranium. For this reason, release of this region is considered vital to maintaining homeostasis in the organism. Although this is a common location to begin to treat headaches, it is also useful in treatment of visceral problems because of its potential influence on the vagus nerve. If this area is addressed with skill, deep relaxation of the patient is quickly achieved. This parasympathetic “relaxation response” is considered to be a healthy and healing alternative to the hypersympathetic overdrive that we tend to exist in as a culture. The origin of this technique dates to the early days of A.T. Still, when he rested his head on a loop of plough rope, fell asleep and awoke to find his headache had been relieved.1 This treatment is performed with the patient in the supine position with the physician at the head of the table as previously described. The fingers of the treating hand make contact with the tissue just under occiput in the tissue of the region of the atlas because the atlas has no definitive landmark as a spinous process. The tips of the fingers are gently extended anteriorly into the muscles of the

Conclusion Osteopathy is a complete system of medicine with a rich history, uniquely American, and full of scientific observations and treatments that were designed to improve the current practice of medicine. Osteopathic manipulative medicine is a highly refined system of treatment principles using a diverse set of styles of treatment from the dramatic to the subtle with all manner of variety in between. This rich compendium of manual medicine has its roots in a mechanistic, newly industrialized world, but also includes a rich spirituality and respect for the inherent miraculous healing ability of the human body. This chapter provides only a cursory overview of this topic and a lifetime of study is necessary to fully appreciate the breadth and scope of the potential effect of what is presently known as osteopathic manipulative medicine. The reader is encouraged to contact the following organizations to obtain further information about their curricula designed

Osteopathic Manipulative Medicine: A Functional Approach to Pain  171

to more completely introduce the concepts, principles, and techniques described in this chapter: American Academy of Osteopathy 3500 DePauw Blvd., Suite 1080 Indianapolis, IN 46268 (317) 879-1881 (317) 879-0563 fax The Cranial Academy 8202 Clearvista Parkway #9-D Indianapolis, IN 46256 (317)-594-0411 (317)-594-9299 fax MSUCOM Office of CME A306 East Fee Hall East Lansing, MI 48824-1316 (800) 437-0001 (517) 353-9714 (517) 432-9873 fax ACKNOWLEDGMENT Special thanks to Robert Baker, DO for his help in preparing this chapter and to Leah Welsh for acting as model for the manipulative medicine photos.

REFERENCES   1. Still AT: Autobiography of A.T. Still. Kirksville, Mo, 1908.   2. Trowbridge C. Andrew Taylor Still, 1828-1917. Kirksville, Mo: The Thomas Jefferson University Press; 1991.   3. Still AT. Philosophy of Osteopathy. 1899.   4. Hildreth AG. The Lengthening Shadow of Dr. Andrew Taylor Still. Kirksville, Mo: Simpson; 1942.   5. Ward RC, ed. Foundations for Osteopathic Medicine. 2nd ed. ­Philadelphia: ­Lippincot Williams & Wilkins; 2003.   6. Johnston WL, Friedman HD, Eland DC: Functional Methods, 2nd ed. Indianapolis, In: American Academy of Osteopathy, 2005.   7. Mitchell FLJ. The Muscle Energy Manual. East Lansing, Mich: MET Press; 1995.   8. Gray’s Anatomy. 40th ed. UK: Elsevier; 2008.

  9. Bhangle SD, Sapru S, Panush RS. Back pain made simple: An approach based on principles and evidence. Cleve Clin J Med. 2009;76:393-399. 10. Beal MC. Viscerosomatic reflexes: A review. J Am Osteopath Assoc. 1985;85:786-801. 11. Kuchera WA, Kuchera ML. Osteopathic Principles in Practice. 2nd ed. Columbus, Ohio: Greyden Press; 1994. 12. Jones LH. Spontaneous release by positioning. The DO. 1964:109-116. 13. Jones LH. Strain and Counterstrain. Newark, Ohio: American Academy of Osteopathy; 1981. 14. Rennie PR, Glover JC, Carvalho C, Key L. Counterstrain and Exercise: An Integrated Approach. 2nd ed. Williamston, Michigan: RennieMatrix; 2004. 15. Howell JN, Cabell KS, Chila AG, Eland DC. Stretch reflex and Hoffmann reflex responses to osteopathic manipulative treatment in subjects with Achilles tendinitis. J Am Osteopath Assoc. 2006;106:537-545. 16. Simons DG, Travell JG. Myofascial Pain and Dysfunction: The Trigger Point Manual. 2nd ed. Baltimore: Lippincott Williams and Wilkins; 1999. 17. English R. The Theory of Technique JAOA. 1920. 18. Johnson SM, Kurtz ME. Osteopathic manipulative treatment techniques preferred by contemporary osteopathic physicians. J Am Osteopath Assoc. 2003;103:219-224. 19. American osteopathic association position paper on osteopathic manipulative treatment of the cervical spine. AAO Newsletter. 2004:15-17. 20. Kimberly PE. Outline of Osteopathic Manipulative Procedures: The Kimberly Manual. In: Millenium, ed. Marceline, Miss: Walsworth Publishing; 2000. 21. Blechschmidt E. The Otogenetic Basis of Human Anatomy; A Biodynamic Approach to Development from Conception to Birth. Berkeley, Cal: North Atlantic Books; 2004. 22. Becker RF. The meaning of fascia and fascial continuity. Osteopathic Ann. 1975:186-196. 23. Magoun HI. Ostoepathy in the Cranial Field. Meridian, Idaho: Sutherland Cranial Teaching Foundation; 1976. 24. Sutherland WG. Teachings in the Science of Osteopathy. Portland, Ore: Rudra Press; 1990. 25. Bibliography of Research Related to Osteopathy in the Cranial Field. Indianapolis, In: Cranial Academy Publishers; 1999. 26. Liem T, McPartland JM, Skinner E. Cranial Osteopathy: Principles and Practice. 2nd ed. China: Elsevier; 2004. 27. Becker RE. Life in Motion. Portland, Ore: Stillness Press; 1997. 28. Dean NA, Mitchell BS. Anatomic relation between the nuchal ligament (ligamentum nuchae) and the spinal dura mater in the craniocervical region. Clin Anat. 2002;15:182-185.

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The Treatment of Pain Through Chinese Scalp Acupuncture

19

Jason Jishun Hao, DOM, MTCM, MBA, and Linda Lingzhi Hao, DOM, PhD

Chinese scalp acupuncture is a contemporary technique combining traditional Chinese needling methods with Western medicinal knowledge of various representative areas of the cerebral cortex. Scalp acupuncture has been proved to be an effective technique for treating acute and chronic pain due to central nervous system disorders ranging from phantom pain and complex regional pain, to strokes and multiple sclerosis. The scalp somatotopic system appears to manifest the convergence of the central nervous system and the endocrine system. The scalp somatotopic system seems to operate as a miniature transmitter-receiver in direct contact with the central nervous system and endocrine system. By stimulating those reflex areas, acupuncture can have a direct effect on the cerebral cortex, cerebellum, thalamo-cortical circuits, thalamus, hypothalamus, and pineal body. Its unique neurologic and endocrinal composition makes the scalp an ideal external stimulating field for internal activities of the brain. Using a small number of needles, scalp acupuncture can often produce remarkable results almost immediately, sometimes taking only several seconds to a minute to complete. Acupuncture, an oriental therapeutic technique, can be traced back more than 2500 years, summarizing centuries of Chinese experience in preventing and treating disease. Throughout its long history, acupuncture has continued to evolve its own unique traditional medicine, forming many new and different methods by embracing newly developed knowledge and technology. Current developments in acupuncture include new acupuncture points and new techniques such as electric and laser acupuncture. One of the most important advancements that ancient Chinese acupuncture has made in the past 60 years has been to create scalp acupuncture by integrating Western medicine into its traditional needling techniques. Scalp acupuncture is well-researched natural science and incorporates extensive knowledge of the past and the present. Years of clinical experience have contributed to the majority of discoveries and developments in scalp acupuncture. This modern system of acupuncture has been formally explored since the 1950s in China, but treatment by needling the scalp and knowledge of scalp acupuncture has been traced back to early civilization. In the first Chinese medicine book, The Emperor’s Internal Medicine described the relationship between brain and body in physiology, pathology, and treatments. Citations of acupuncture treatments on the head are also found throughout classical Chinese literature. Around 1950, various famous Chinese physicians introduced Western neurophysiology into acupuncture fields and explored the

relationship between the brain and human body. Although there were several hypotheses, it took acupuncture practitioners roughly 20 years before they accepted a central theory that incorporated brain functions into the Chinese meridian theories. Dr. Jiao Shunfa, a neurosurgeon in Shanxi province in China, is the official recognized founder of Chinese scalp acupuncture.1 Starting in 1972, he systematically undertook the scientific exploration and charting of scalp correspondences for the first time in more than 2500 years of acupuncture history. Dr. Jiao combined a modern understanding of neuroanatomy and neurophysiology with traditional techniques of Chinese acupuncture to develop a radical new tool for treating the central nervous system. At the time, scalp acupuncture was primarily used to treat paralysis and aphasia due to stroke. Dr. Jiao’s discovery was investigated, acknowledged, and formally recognized by the acupuncture profession in a national unified acupuncture textbook, Acupuncture and Moxibustion in 1977. In 1987, scalp acupuncture began to gain international recognition at the first International Acupuncture and Moxibustion Conference held in Beijing. In 1989, Dr. Jason Jishun Hao brought scalp acupuncture to the United States. Since then, Dr. Hao has trained hundreds of acupuncture practitioners and treated thousands of patients with disorders of the central nervous system in the United States. After its introduction in the United States, the techniques and applications of scalp acupuncture have been expanded and developed through further research and experience. Studies and research on scalp acupuncture continue to show positive results in treating the disorders of the central nervous system.2 Scalp acupuncture is different from traditional acupuncture in its fundamental theories, locations, stimulation techniques, and patient’s responses. Scalp acupuncture treats and prevents disease through the proper insertion of needles into scalp areas. It is accompanied by different manipulations to regulate and harmonize the functional activities of the brain and body, as well as to restore and strengthen the functions of the body, organs, and tissues. Scalp acupuncture is based on a reflex somatotopic system organized on the surface of the scalp. Scalp acupuncture consists of needling areas versus points on the skull according to the brain’s neuroanatomy and neurophysiology. Unlike acupuncture, where one needle is inserted into a single point, in scalp acupuncture needles are subcutaneously inserted into whole sections of various zones. These sections are the specific zones through which the functions of the central nervous system, endocrine system, and meridians are transported to and from the surface of the scalp. 173

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From a Western perspective, these areas correspond to the cortical areas of the cerebrum and cerebellum, which are responsible for central nervous system functions such as motor function, speech, and balance (Figs. 19-1 and 19-2). In clinical practice, acupuncture treatments are typically based on highly individualized philosophical constructs, and the practitioner has a wide amount of discretion on the type of points and techniques. Therefore, even when treating the same complaint, the method of treatment chosen by one practitioner can vary significantly from another. Scalp acupuncture, on the other hand, applies more of a Western medicine approach in which patients with the same diagnosis usually receive similar types of treatments. In various cases, scalp acupuncture has not only been proved as a more effective treatment for many diseases in the central nervous system, it is also more easily accessible, less expensive, entails less risk, can yield quicker responses, and often causes fewer side effects than some Western treatments. In a recent study by the author, scalp acupuncture was used to treat seven patients with phantom limb pain at ­Walter Reed Army Medical Center in Washington, D.C.3 After only one treatment per patient, three of the seven patients instantly felt pain relief and showed significant improvement, whereas three patients showed some improvement, and only one patient showed no improvement (see later). Because of the limited numbers of patients, this needs to be replicated on a larger scale. It ­nevertheless shows the potential efficacy of scalp acupuncture in treating phantom pain. The technique of scalp acupuncture is systematic, logical, and relatively easy to understand and practice. The techniques introduced in this chapter can be performed even if one has

Motor cortex

little acupuncture experience. Scalp acupuncture treatment can be used as the primary approach or as a supplement to other acupuncture modalities. Scalp areas are frequently used in pain management, especially pain caused by the central nervous system such as phantom pain, reflex regional pain, and residual limb pain. Scalp acupuncture is also often used in the rehabilitation of paralysis due to stroke, multiple sclerosis, automobile accident, and Parkinson disease. It has been proved to have effective results in treating aphasia, loss of balance, loss of hearing, dizziness, and vertigo. In the West, although scalp acupuncture has been known for some time, the technique has been taught and used only sparingly. Only a handful of books with scalp acupuncture as the main emphasis have been published. With such little information available, it is almost impossible to apply this technique in practice. In the West, most healthcare practitioners are familiar with acupuncture for pain management. However, scalp acupuncture, as a tool for paralysis rehabilitation, is a relatively new concept. Even now, it is not surprising for a Western physician to claim that it is a coincidence if a patient recovers from paralysis after acupuncture. Therefore, there is an urgent need for Chinese scalp acupuncture to be developed, studied, and expounded by modern science and technology. Much more research needs to be done on scalp acupuncture so that its potential can be fully explored and utilized. Scalp acupuncture can provide solutions in situations where Western medicine solutions are limited or entail too much risk. This chapter will show the scope of scalp acupuncture in treating many kinds of diseases. This research is derived from many years of clinical experience and can be used as the foundation for future clinical practice and research.

Sensory cortex

Association cortex

Association cortex

Broca’s area

Association cortex

Motor cortex

Broca’s area Sensory cortex Auditory cortex

Auditory cortex Visual cortex Association cortex

Wernicke’s area Cerebellum

Figure 19-1  Cerebral cortex, side view. (Courtesy Jason Jishun Hao.)

Wernicke’s area

Visual cortex

Figure 19-2  Cerebral cortex, top view. (Courtesy Jason Jishun Hao.)

The Treatment of Pain Through Chinese Scalp Acupuncture  175

Location and Indication Precise location of Chinese scalp acupuncture areas requires identification of two imaginary lines on the head. The anteriorposterior line runs along the centerline of the head. The midpoint of the skull is located at the midpoint between the occipital protuberance and the glabella, midway between the eyebrows. The second line, the horizontal line, runs from the highest point of the eyebrow to the occipital protuberance. Where this line intersects the anterior hairline defines the lower point of the motor area (Fig. 19-3). In patients without a definite hairline, an alternative method for locating this point is to draw a vertical line up from acupuncture point ST-7 until it intersects the line from the brow to the occipital.

Motor Area Location The motor area is located on the projective area of the scalp corresponding to the precentral gyrus of the frontal lobe. The motor area is located in a strip beginning at the midline at a point 0.5 cm poster­ ior to the previously located midpoint of the head, along the anterior-posterior line.4 The motor area runs from this point obliquely down to the point where the eyebrow-occipital line intersects the anterior hairline (Fig. 19-4). The line of the motor area determines the angle and location of several other areas, such as the sensory area and chorea and tremor area. The motor area of the cerebral cortex controls and adjusts intersectional body movements. One side of the cerebral cortex controls contralateral muscles of the body in the level below the

Midpoint of midline 0.5 cm behind midpoint

Midpoint of eyebrow

neck. One exception is that most head and face muscles are bilateral. The size of the motor gyrus of the cerebral cortex is associated with complexity and accuracy of body movement. A larger representative area equates to greater complexity and accuracy. The motor gyrus is depicted as an upside-down human body image. For example, the upper part of the gyrus controls the lower limbs, whereas the middle part of the gyrus controls upper limbs, and the lower parts control head and face movement. The motor area is divided into three regions according to the homunculus projection.5 In order to correctly locate those three regions, the whole motor area is first equally divided into fifths. Then three regions are measured as Upper one-fifth region, Middle two-fifths region, and Lower two-fifths region. The Upper one-fifth region is used to treat contralateral movement dysfunction of the lower extremity, trunk, spinal cord, and neck. The Middle two-fifths region is used to treat contralateral movement dysfunction of the upper extremity. The Lower two-fifths region is used to treat bilateral movement dysfunction of the face and head. These areas are used to affect the contralateral side of the body. The direction of needling is usually from the upper part of the area downward, penetrating to the entire area.

Motor Area Indications Indications to apply needles in the motor area are: paralysis or weakness in the face, trunk, or limbs caused by stroke; multiple sclerosis; traumatic paraplegia; acute myelitis; progressive myotrophy; neuritis; poliomyelitis; post-polio syndrome; periodic paralysis;

Blood vessel dilation and constriction area

Chorea and tremor control area Motor area Sensory area

Voluntary movement area

1/5

Speech II area Speech I area Vertigo and hearing area

2/5

Glabella 2/5

Speech III area

Occipital protuberance

Intersection between eyebrow-occiput line and hairline Motor area measurements Figure 19-3  Lower point of the motor area. (Courtesy Jason Jishun Hao.)

Stimulation areas - side view Figure 19-4  The motor area runs from this point obliquely down to the point where the eyebrow-occipital line intersects the anterior hairline.   (Courtesy Jason Jishun Hao.)

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hysterical paralysis; Bell’s palsy; spinal cord injury; traumatic brain injury; and brain surgery. Among the disorders mentioned earlier, the most common problems are generally paralysis due to stroke, multiple sclerosis, and traumatic injury. When treating a thrombosis and embolism stroke, scalp acupuncture treatment should begin as soon as possible. When treating a hemorrhagic stroke, scalp acupuncture treatment should not be performed until the patient’s condition is stable, typically at least 1 month after the stroke. Although stroke can be treated at any stage, the greatest response to treatment will be for strokes occurring less than a year prior to scalp acupuncture. The longer the duration of the impairment, the more gradual the improvement will be. With long-term cases of impairment, expectations need to be realistic, although some patients will occasionally surprise practitioners. Improvement is rare for patients with a long history of paralysis that has led to muscular atrophy, rigid joints, and inflexibility. When treating chronic progressive diseases like multiple sclerosis and Parkinson’s, the results from treatment are sometimes temporary. Results may last for hours, days, weeks, or months, but ongoing follow-up treatments will be necessary. However, when treating paralysis from either stroke or trauma, the improvements of movement are often permanent. Although each part of the cerebral cortex has its own functions, it is relative to our understanding of brain functions. When one area is impaired, the impaired area can recover to a limited extent. In addition, by employing proper stimulation, other areas can compensate for the impaired area. This may be the answer to explaining the mechanism of scalp acupuncture in treating cerebral cortex impairment. Generally speaking, paralyzed extremities are targeted by treating the opposite site of the motor area in the scalp. For instance, if a patient has paralysis of the right leg and foot, needles should be inserted into the patient’s left side of the scalp motor area. However, for patients undergoing brain surgery or with an injury where part of the brain was removed, needling should be on the same side of the scalp as the side of the paralyzed limb. For treating motor dysfunction, place the needles and rotate them at 200 times per minute for 2 to 3 minutes every 10 minutes for a total of 30 to 60 minutes. More difficult cases require longer treatment times. For the best results, the patient should feel something in the reference area: tingling, movement, twitching, heat, cold, and so on. After stimulating the needles, begin passive and active movement of the affected limbs. It is helpful to have the patient walk, with or without assistance as indicated, between stimulations. Initially, the treatment should be twice a week until major improvements are achieved, then once weekly, then every 2 weeks, and then spaced out as indicated by the patient’s condition.

Sensory Area Location The sensory area is located on the projective area of the scalp corresponding to the post-central gyrus of the frontal lobe. The sensory area is one of the most commonly used in Chinese scalp acupuncture. It is located parallel to the motor area, 1.5 cm posterior to the motor area (see Fig. 19-4). The sensory area of the cerebral cortex controls and adjusts sensation in the opposite side of the body. One side of the cerebral cortex controls contralateral sensation of the body in the level below the neck. One exception is that most of the sensation of the head and face are bilateral. The sensory gyrus, like the motor gyrus, is also distributed as an upside-down human body image. That means the upper part of the gyrus controls the lower limbs; the

middle part dominates the upper limbs; and the lower part controls head and face movements. The sensory area is also divided into three regions according to the homunculus projection. These are the same proportions as discussed for the motor area: the Upper one-fifth, the Middle twofifths, and the Lower two-fifths. These zones follow the same distribution, with the lower extremity, trunk, and neck in the Upper Zone, the upper extremity in the Middle Zone, and the face and head in the Lower Zone. These areas are used to affect the contralateral side of the body. The direction of needling is usually from the upper part of the area downward, penetrating the entire area.

Sensory Area Indications Indications to apply scalp acupuncture to the sensory area are: abnormal sensations of face, trunk, and limbs that are either hyposensitive or hypersensitive including pain, tingling, numbness; and loss of ­sensation in the contralateral side of the body. The following disorders have shown positive results when treated by scalp acupuncture: loss of sensation or pain from stroke and traumatic injury, numbness and tingling from multiple sclerosis, phantom pain, complex regional pain, residual limb pain, trigeminal neuralgia, temporomandibular joint dysfunction (TMJ), migraine headache, cluster headache, shingles, pain in the neck, shoulder, back and lower back, sciatica, gout, plantar fasciitis, fibromyalgia, neuropathy, and paresthesia. In general, abnormal sensations of an extremity are treated by choosing the opposite site of the sensory area in the scalp. For instance, if a patient has pain in the right leg and foot, the left side of the sensory area in the scalp should be needled. However, for patients having brain surgery and an injury where part of brain was removed, needles should be placed on the same side of the scalp as the affected limb. For example, a patient with numbness in the left leg and foot, would be treated with needles on the left side of the scalp’s sensory area. Scalp acupuncture produces excellent results for pain, numbness, and tingling. Many patients show significant improvement during initial treatment. Scalp acupuncture results in much quicker effects compared to other modalities of acupuncture, such as in the ear, hand, or body. Some patients felt improvement just a few seconds or a few minutes after their scalps were needled. As with the motor area, the Upper one-fifth of the sensory area is used to treat abnormal sensation and pain in the lower extremities, trunk, back, chest, and neck. The Middle two-fifths is used for the upper extremities. The Lower two-fifths is used for problems with the face and head, including migraines, headaches, trigeminal neuralgia, toothache, and TMJ.

Additional Areas of the Cortex Tremor and Chorea Area The tremor and chorea area is located on the projective area of the scalp corresponding to the basal ganglion area. This gyrus has important motor-adjusting functions that closely involve stability of voluntary movement and the control of muscular tension. The Chorea and Tremor Area is located parallel to the motor area, 1.5 cm anterior to the motor area (see Fig. 19-4). It runs 4 cm and starts 1 cm anterior to the Midpoint at its upper point. This area is always needled bilaterally and is used for any involuntary motor activity. This is the primary area for the treatment for Parkinson’s disease, tremor, shaking of the head, body, or extremities, and chorea. This area is also very effective for treating patients with muscular tension and tightness in any part of the body. The direction

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of needling is usually from the upper part of the area downward, penetrating to the entire area. Vascular Dilation and Constriction Area This area is also parallel to the motor area, 1.5 cm anterior to the chorea and tremor area, or 3 cm anterior to the motor area (see Fig. 19-4). This area is also always needled bilaterally and can be used for essential hypertension, cortical edema, and other autonomic vascular dysfunctions. The direction of needling is usually from the upper part of the area downward, penetrating the entire area. Vertigo and Hearing Area This area is located over temporal lobe in the lateral side of the head. It is on the horizontal line and totals 4 cm.6 It starts 1.5 cm superior to the apex of the auricle of the ear at its middle point, and extends 2 cm anterior and 2 cm posterior to the middle point (see Fig. 19-4). This area is also needled bilaterally and can be needled in either direction. This is a very useful area for treating vertigo, dizziness, Meniere disease, tinnitus, hearing loss, and hearing hallucination. Speech I Area There are three speech areas. Speech I area is located in the posterior third of the gyrus frontalis inferior over the frontal lobe, and controls groups of muscles for speech and phonation. Speech I area corresponds to Broca’s speech area of the frontal lobe, which controls the muscles of the tongue and mouth that form speech. Speech I area overlaps the lower 2/5 40% of the motor area (see Fig. 19-4). The major indication for Speech I is in the presence of motor aphasia after stroke or brain injury, where the muscles of speech and vocalization have been paralyzed. This area is needled bilaterally for motor aphasia. The direction of needling is usually from the upper part of the area downward, penetrating the entire area. Speech II Area This area lies over the reading and comprehension part of the parietal lobe, and is located by finding the parietal tubercle. From the parietal tubercle, run a line parallel to the anterior-posterior line 2 cm posteriorly. Using this as the starting point, the Speech II area runs 3 cm in length, parallel to the anterior-posterior line (see Fig. 19-4). This area is used bilaterally for nominal aphasia—the inability to name objects. In this disorder, the patient can describe an object, but cannot produce the noun. The direction of needling is usually from the upper part of the area downward. Speech III Area This overlies Wernicke’s area of the temporal lobe, and overlaps the posterior half of the vertigo and hearing area. It lies on the same horizontal line 1.5 cm superior to the apex of the auricle but begins at the midpoint of the vertigo and hearing area directly above the auricle and runs 4 cm posteriorly (see Fig. 19-4). It is used bilaterally for treatment of expressive aphasia, where the patient can articulate words, but the words don’t make sense. The direction of needling can go either from the left part to the right or from right to left side, penetrating the entire area. Praxis Area This is an area used uncommonly. Starting from the parietal tubercle, the praxis area joins three lines, one running straight downward, and the other two at a 40-degree angle anterior and posterior to the vertical line (see Fig. 19-4). This area is used for apraxia—the inability to execute certain fine motor activities such as buttoning a shirt.

Vision Area The vision area is located over the occipital lobe on the posterior aspect of the head. It starts on a horizontal line at the level of the occipital protuberance. The vision area starts at a point 1 cm lateral to the occipital protuberance and runs upward for 4 cm, parallel to the anterior-posterior line (Fig. 19-5). The vision area is often needled bilaterally. Unlike other scalp areas in Chinese acupuncture, the vision area must be needled from the top down. Needling from below upward incorrectly has the risk for causing injury to the medulla. Indications for needling are vision loss due to stroke or brain injury, visual field loss, visual hallucination, and nystagmus. Balance Area The balance area is located over the cerebellum. It starts on a horizontal line at the level of the occipital protuberance. The balance area starts from a point 3.5 cm lateral to the occipital protuberance and runs 4 cm inferiorly (see Fig. 19-5). Both the vision and balance areas are needled bilaterally. These are the only areas that must be needled from the top down. Indications for needling the balance area are disequilibrium, cerebellar atrophy, cerebellar strokes, multiple sclerosis, Parkinson’s disease, ataxia, and loss of balance due to traumatic brain injury. Foot Motor and Sensory Area (FMSA) The foot motor and sensory area is the most commonly used one in Chinese scalp acupuncture. It has broad-ranging effects on both motor and sensory functions. The FMSA is located parallel to the anterior-posterior line, 1 cm lateral to the midline beginning at the level of the midpoint of anterior-posterior line and running 4 cm posteriorly (Fig. 19-6). The foot motor and sensory area gets its

Foot motor and sensory area

Speech II area Vision area

Balance area

Figure 19-5  Stimulation area, back view. (Courtesy Jason Jishun Hao.)

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name from including both the motor area and the sensory area in the region of the foot on the homunculus. Although it is useful for motor and sensory problems of the feet, the foot motor and sensory area has a much broader effect and is used for a wide-ranging collection of symptoms. Because the area overlies many endocrine glands, such as the pituitary gland and adrenal gland, it not only affects the central nervous system but also regulates the endocrine system. That is why the FMSA can treat many kinds of different disorders. The foot motor and sensory area is usually needled bilaterally, either from the front part of the area to the back part or vice versa. However, it is relatively easier if the direction is from front to back. Indications for needling the foot motor and sensory area are: paralysis of the leg or foot, restless leg syndrome, pain in legs and feet including gout, neuropathy, plantar fasciitis, reflex sympathetic dystrophy or complex regional pain, fibromyalgia, phantom pain, residual limb pain, numbness and tingling in legs and feet, pain in the neck and shoulders, incontinence of urine, bedwetting, incontinence of stool, irritable bowel syndrome, impotence, premature ejaculation, decreased libido, infertility, prolapse of the uterus, amenorrhea, dysmenorrhea, abnormal uterine bleeding, psoriasis, neurodermatitis, shingles, attention deficit hyperactivity disorder (ADHD), posttraumatic stress disorder, postconcussion syndrome, poor memory, poor concentration, emotional disturbances, and mental retardation. Avoid needling the Foot Motor and sensory area in pregnancy because there is a theoretical risk of inducing uterine contractions. Internal Organ Areas The internal organ areas are located on the front of the head. The location of internal areas is based on clinical experience versus anatomy and physiology as known in Western medicine. These scalp areas are not used often because traditional body acupuncture produces excellent results.

Head Area The head area is located on the midline at the forehead, running from the hairline 2 cm superiorly and inferiorly (Fig. 19-7). This area is used for treating mental and emotional disorders, such as insomnia, poor memory, poor concentration, anxiety, and depression. Thoracic Cavity Area This is located half the distance between the stomach area and the midline, running from the hairline 2 cm superiorly and inferiorly (See Fig. 19-7). This area is used for treating asthma or tachycardia. Stomach Area This is located on the midpupillary line from the hairline 2 cm superiorly (see Fig. 19-7). This area is used for treating stomach pain and discomfort in the upper epigastric region. Liver and Gallbladder Area The liver and gallbladder line descends onto the forehead for 2 cm along the midpupillary line (see Fig. 19-7). This area is used for treating costal pain and rib pain due to hepatitis, gallstone, and shingles. Reproductive Area This area starts at the frontal corner of the hairline, running 2 cm superiorly (see Fig. 19-7). It is useful for treating menstrual cramps, bleeding, and urinary tract infections. Large Intestine Area This descends onto the forehead for 2 cm along the reproductive line (see Fig. 19-7). The area can be used in cases of diarrhea or constipation.

Head area

Thoracic cavity area Stomach area

Liver and GB area Midpoint of midline

Upper point of motor area

Intestines area

Reproduction area

Foot motor and sensory area

Foot motor and sensory area Upper point of sensory area

Figure 19-6  Stimulation area, top view. (Courtesy Jason Jishun Hao.)

Figure 19-7  Stimulation area, front view. (Courtesy Jason Jishun Hao.)

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Needle Techniques Insertion of the Needle The needle should be inserted by using the free hand technique instead of a guide tube, which is a popular insertion technique in the West. This is because of the special anatomy of the scalp consisting of five layers: skin, connective tissue, aponeurosis, loose areolar tissue, and pericranium. In Chinese scalp acupuncture, a 30 to 36 gauge stainless steel acupuncture needle with a length of 1.5 inches is placed in the loose areolar tissue layer beneath the aponeurosis and above the pericranium. To place the needle correctly, hold the needle with the nondominant hand. Place the tip at a 15 to 25-degree angle to the skin. Use the dominant hand to quickly pierce the skin and thread the needle through the loose areolar tissue layer for the entire length of the needle, 1 to 2 inches deep. The proper angle, depth, and speed of inserting needles reduces sensations of pain and discomfort significantly. While the needle penetrates the skin, the practitioner’s fingers will have a sense of slight tightness at first. When the needle reaches the loose areolar layer, the practitioner’s fingers will feel the tightness disappear or reduce. Once the layer becomes looser, the needle will smoothly push deeper, with little or no resistance. At this time, push the needle to the designed depth as quickly as possible. It only takes 1 to 2 seconds for an experienced practitioner.

Manipulation Once the needle is in the correct position, the needle is stimulated with manual manipulation. Grasp the handle of the needle between the thumb and the distal interphalangeal joint of the index finger. By moving the index finger and keeping the thumb stationary, you can twirl the needle at a rate of 200 to 400 times per minute. Rotate clockwise and counter-clockwise with amplitude ranging from 360 to 720 degrees. In other words, make 1 to 2 turns in each direction. Rotate needles every ten minutes for 2 to 3 minutes. Electronic stimulation may be used to replace hand stimulation. It can strengthen the stimulation and improve the therapeutic effect for the novice who cannot rotate needles at the minimum of 200 times per minute. If this method is chosen, a pair of needles is connected to the electronic stimulator. For scalp acupuncture the negative lead form the stimulating device is connected to the secondary area, and the positive lead is connected to the primary stimulating area on the scalp. The recommended frequency is in the 3 to 4 Hz range— approximately equal to 200 times per minute. The ideal intensity should be at the level that the patient can feel without causing any pain. The duration of the electrical stimulation is ten to twenty minutes.

Timing and Frequency of Treatment The needles are stimulated for approximately 2 minutes and restimulated at 10-minute intervals over the course of treatment. Most treatments of scalp acupuncture last 30 to 45 minutes. In China and other Asian countries, patients are usually treated every day if they are in the hospital. Cost of acupuncture in Asia is inexpensive compared to Western countries and it is very convenient for acupuncture treatments when patients are in hospital. According to the authors’ experience, two or three treatments per week are cost efficient and effective for patients who are not hospitalized; these patients can recover as quickly as if they are treated every day.

Withdrawing the Needle Needle removal is accomplished with one swift motion by pressing down the hair around the needle with one hand. Meanwhile, hold the needle between the thumb and index finger of the other hand. Rotate the needle gently to make sure it is loose, then withdraw it quickly. After that, press the needling area with a dry cotton ball for a short while to prevent bleeding. Because of the scalp’s rich blood supply, the needled sites bleed more frequently on removal of the needle than at other body sites. It is therefore important to press the needled site a little longer and recheck it after removing the cotton ball.

Contraindication and Precaution It is inadvisable to apply scalp acupuncture on any scalp area where there is infection, ulcer, tumor, or postoperative skull defect. Also it is inadvisable to treat an infant whose fontanel has not yet closed. The same contraindications hold as for other acupuncture. Do not use scalp acupuncture on patients with a tendency to hemorrhage, or on those with severe hypertension, high fever, or an acute stage of cerebral hemorrhage.

Clinical Applications and Case Studies As mentioned earlier, scalp acupuncture is highly effective for managing many types of pain, based on 37 years of experience and studies in China, as well as the authors’ own 27 years of practice. This section will present those disorders that have outstanding results from treatment by scalp acupuncture.

Phantom Limb Pain, Residual Limb Pain, and Complex Regional Pain Phantom limb pain, residual limb pain, and complex regional pain are common symptoms for patients with limb injuries and/or amputations. Several studies have shown that approximately 70% to 80% of patients develop pain within the first few days after amputation. Phantom limb pain is the term for abnormal sensation perceived from a previously amputated limb.7 Patients may feel a variety of sensations emanating from the absent limb. The limb may feel completely intact despite its absence. Patients often describe their pain as burning, squeezing, cramping, prickling, shooting, or stabbing sensations. Residual limb pain is believed to come from injured nerves at the amputation site. Residual limb pain is often associated with phantom limb sensation and pain, and may be related in etiology. Complex regional pain is a “chronic pain syndrome with severe pain, changes in the nails, bones, skin, and an increased sensitivity to touch in the affected limb.” The former term for this was reflex sympathetic dystrophy. Several theories have been proposed regarding the cause of phantom limb pain. An understanding of the mechanisms underlying phantom pain is likely to lead to new and logical types of treatments. Some studies have indicated that phantom pain might originate in the brain. Other areas of the brain fill in when the area of the brain that controlled the limb no longer has a function after amputation. There is a reorganization of the primary sensory cortex, subcortex, and thalamus after amputation. The reorganization of the sensory cortex is currently considered to be responsible for phantom limb pain.

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Conventional medicine has provided limited help in alleviating these types of pains. Acupuncture, on the other hand, is becoming a more popular method of treatment for acute and chronic pain. It ranks high among nonmedical treatments such as transcutaneous electrical nerve stimulation, vibration therapy, biofeedback, hypnosis, massage, physical therapy, and electroconvulsive therapy. Scalp acupuncture has been proved to be the most effective technique for treating central nervous system damage. This treatment is indicated when there is phantom limb pain, residual limb pain, complex regional limb pain, postconcussion syndrome, or posttraumatic stress disorder. In these cases, scalp acupuncture is superior to needling on the body, ear, or hand. The areas recommended for scalp acupuncture are: sensory, leg motor and sensory, tremor, and motor area. The foot motor and sensory areas are the primary locations to treat limb pain. The sensory area is an important treatment location. The Upper one-fifth of the sensory area is unilaterally selected to treat opposing leg and foot pain. The Middle two-fifths of the sensory area is unilaterally selected to treat opposing arm and hand pain. The Lower two-fifths of the sensory area is bilaterally selected to treat facial and ear pain. Tremor areas are classified as secondary locations to treat limb pain and are bilaterally selected to treat spasm pain on either or both sides. Proper manipulation techniques are crucial to obtaining the desired results. The needles are usually retained for 30 to 45 ­minutes with stimulation every 1 to 2 minutes using a rotational technique every 10 minutes. The patients are often treated two to three times a week, depending on the degree of pain. Although there are certainly other acupuncture techniques, such as on the ear and body, scalp acupuncture is a more effective method; it results in more rapid and often immediate pain relief. Scalp acupuncture was applied to treat seven patients with limb pain at Walter Reed Army Medical Center in Washington, D.C. on February 11 and 12, 2006. After only one treatment for each patient, three of seven patients instantly felt pain relief and showed significant improvement, three patients showed some improvement, and only one patient showed no improvement. The subsequent cases are from treatments at Walter Reed Army Medical Center. Case Report 1—Phantom Pain Several months after both legs were amputated, the patient still felt severe phantom pain. Various types of medication provided little relief. The pain interrupted his sleep and caused loss of emotional control. The patient described severe painful tingling sensations in both his feet, with his right foot more painful than the left. As soon as he underwent scalp acupuncture treatment, the patient started to feel heat sensations in both his legs, followed by a tingling almost like an electrical sensation in his toes. Five minutes later, his phantom pain diminished considerably. After ten minutes passed, his phantom pain had completely disappeared. The patient was worried that the pain might recur after the needles in his scalp were removed. He insisted on sitting in the room for a period after he finished the treatment. He was happy to leave the treatment room without any phantom pain 2 hours after his first scalp acupuncture treatment. Case Report 2—Residual Limb Pain This patient experienced severe residual limb pain in his right stump immediately after surgery 5 months previously. He described the chronic pain like the presence of “a wire tight up his leg” with spasms that resulted in an intolerable state of pain. Scalp

acupuncture was applied at the foot motor and sensory area, and Upper one-fifth sensory area. Fifteen minutes after four needles were inserted in his scalp, followed by stimulation of the needles by the clinician, the patient felt a numb and tingling sensation in his leg. After this, the sensation of tightness in the leg began to lessen. After 5 more minutes, the tight leg spasm and pain were nearly gone. Case Report 3—Complex Regional Pain After being shot twice in each leg during a battle in Iraq, this patient suffered from severe complex regional pain in his right leg. His right leg and foot were so sensitive that even the lightest touch or contact from a thin blanket or a sock would induce pain so severe that the patient could hardly tolerate it. The patient lost his ability to stand and walk because of sensitivity of the right foot. As soon as the needles were inserted in his scalp, the patient experienced a “water bubble-like sensation.” First the sensation moved from his right hip to his leg, then to his foot and toes. Five to eight minutes later, his leg and foot pain started to diminish and he was able to make contact with his leg and toes with little discomfort. The patient was so excited to feel the results that he continued to touch his leg and toes to verify that they really were better. He was asked to try to put a sock on his right foot and he did so without showing pain or discomfort. The patient then proceeded to take a short nap. At the follow-up visit the next day, the patient was lying on the bed with both socks on. He had very little pain and was much less sensitive than before. He was able to walk with almost no pain after four needles were placed in his scalp. Each step he took brought on applause from observers.8 Although few scientific investigations have directly assessed the efficacy of scalp acupuncture treatment in limb pain, this study at Walter Reed Hospital, showed that the patients instantly felt effectiveness with only one treatment. Scalp acupuncture treatment for pain relief is accessible and safe; it is less expensive than pain medications and has fewer side effects. In the future, it would be helpful to conduct controlled studies of effectiveness of such treatment. Scalp acupuncture not only benefits patients with limb pain, but also significantly contributes to our understanding of phantom pain. Scalp acupuncture may help investigators to discover the mechanisms of phantom limb and residual limb pain and could lead to the discovery of further advancements in pain management.

Stroke Stroke is the third leading cause of death in the United States, after heart attack and cancer, and it is a leading cause of adult disability. Stroke patients must receive emergency treatment with Western medicine. It is important to identify a stroke condition as early as possible because patients who are treated earlier are more likely to survive and become less disabled. Stroke survivors usually have some degree of sequelae of symptoms depending primarily on the location in the brain involved and the amount of brain tissue damaged. Disability affects about 75% of stroke survivors, and it can affect patients physically, mentally, emotionally, or a combination of all three elements. The symptoms of stroke depend on the type of stroke and the area of the brain affected. They include paralysis, weakness or abnormal sensations in limbs or face, complex regional pain, aphasia, apraxia, altered vision, problems with hearing, taste, or smell, vertigo, disequilibrium, altered coordination, difficulty swallowing, and mental and emotional changes.

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Because each side of the brain controls the opposite side of the body, a stroke affecting one side of the brain results in neurologic symptoms on the other side of the body. For example, if the stroke occurs in the motor area of the right side of the brain, the left side of the body may show weakness or paralysis. Although there is no cure for stroke, most stroke patients now have a good chance for survival and recovery. When stroke patients pass the acute stage, they should start rehabilitation as soon as possible. Stroke rehabilitation is the process by which patients undergo treatment to help them return to their normal life as much as possible by regaining and relearning the skills of everyday living such as speaking or walking. These treatments include acupuncture, physical therapy, occupational therapy, speech and language therapy, and massage. Scalp acupuncture has been found to have a very good effect on the sequelae of stroke, including hemiplegia, aphasia, complex regional pain, and abnormal sensations in the limbs. Many patients treated with scalp acupuncture at our clinics have shown some immediate improvement from their initial scalp acupuncture treatment. Numerous studies in China over the past three decades have shown that scalp acupuncture is effective in relieving the sequelae of stroke, especially for paralysis. Thanks to advanced stroke research and brain imaging technology, physicians continue to gain a new understanding of how the brain can adapt after stroke to regain its ability to function. New research suggests that normal brain cells are highly adaptable and can undergo changes not only in function and shape but also changes that allow them to take over the functions of nearby damaged cells. As a result, scalp acupuncture is geared toward stimulating and restoring affected brain tissue or retraining unaffected brain tissue to compensate for the lost functions of damaged brain tissue. In patients with paralysis or weakness of limbs, the scalp areas for motor, sensory, and speech functions should be treated. If paralysis is in the upper limb, the Upper one-fifth of the motor area should be chosen; if in the leg and foot, the Middle two-fifths of the motor area should be the choice; and if in the face, the Lower twofifths of the motor area should be selected. If there is reflex sympathetic dystrophy, tingling, numbness, or other abnormal sensations in the leg and foot, arm and hand, or face, use the Upper one-fifth sensory area, Middle two-fifths sensory area, and Lower two-fifths sensory area, respectively. The chosen insertion area should be the opposite of the affected limb. For example, if there is paralysis in the right arm, the left Middle two-fifths motor area should be selected. Speech I area is effective for patients with expressive aphasia; speech II area is for nominal aphasia; and speech III is for receptive aphasia. Rotate needles at least 200 times per minute with thumb and index finger for 1 to 3 minutes. The doctor should twirl the needle as vigorously as the patient can tolerate; and have the patient move the affected limb actively and passively. Repeat the stimulation every 10 minutes. During the treatment, patients may have some or all of the following sensations: hot, cold, tingling, numbness, heaviness, distention, or sensations of water or electricity moving down the affected limb. Those patients usually respond and show improvement more quickly. However, those who do not have such sensations could still have immediate positive results. Keep the needles in for 30 to 45 minutes. The patient is given two to three treatments per week, and a therapeutic course consists of 10 treatments. There are many different acupuncture techniques to treat paralysis. Although scalp acupuncture has the fastest response, other techniques are necessary for a fuller recovery. According to the individual’s condition, recovery time can be accelerated by

combining scalp acupuncture with regular body acupuncture, electric acupuncture, and moxibustion (a traditional Chinese medicine technique that involves the burning of mugwort, a small, spongy herb, to facilitate healing), as well as physical therapy and massage. Regular acupuncture treatment has been found to have a positive therapeutic effect on the recovery of movement of hands, fingers, feet, and toes. In treating unilateral paralysis of the limbs, tradition says to select more points from Yang Ming channels because Yang corresponds to movement and agility, and Foot Yang Ming/stomach controls the functions of the muscles. Commonly used points are LI-4, TW-5, LI-11, LI-14, and LI-15 for upper limb paralysis; and UB-60, UB-57, GB-34, ST-36, and GB-30 for lower limb paralysis. Although more Yang Ming points are used for paralysis, points from Yin channels, especially Taiyin and Jueying channels, should not be ignored. Yin corresponds to nourishing muscles and tendons; and those points from Yin channels have positive results for pronounced stiffness and contraction of the limbs. Commonly used points are Lu-5 and P-6 for upper limb and Sp-6, Sp-9, Sp-10, and Li-8 for lower limb. Electrical stimulation is helpful if the practitioner has difficulty performing the rotation of the needle more than 200 times per minute. It is suggested that only two of the scalp needles be stimulated at any one session, or the brain can become too confused to respond. For electrical stimulation in body acupuncture, fewer than four needles should be stimulated in each limb. Best results are achieved when applying low frequency with high intensity. Moxibustion can enhance the therapeutic results of scalp acupuncture, especially for older or weaker patients. The practitioner should consider scalp acupuncture as the primary approach, rather than a complementary approach to the patient with paralysis. Case Report 4—Stroke Maria, a 69-year-old female, was waiting at her home for a scalp acupuncture treatment. Maria was partially paralyzed on her left side after her first stroke 6 years ago. She had a second stroke 3  years later, and she now suffered from aphasia. Her daughter reported that the entire left side of her body was completely paralyzed; and that she had severe spasms and pain in her left arm and leg that caused her enough agony to scream frequently. After her second stroke, Maria had twenty body acupuncture treatments that resulted in little response or improvement. On examination, the patient’s mind was clear when responding to the questionnaire. Although she could make sounds in response to questions, her speech was unintelligible. Maria’s left limbs showed no positive movements at all. They were very stiff and tight, and she could hardly be moved by another person. Her tongue was red with a little coating, and her pulse was wiry and thready. Maria had a positive response to her first scalp acupuncture treatment. After the needles were inserted in her scalp, the spasms, stiffness, and tightness in her left arm and leg showed immediate improvement. Her left limbs became looser, and her daughter was able to move Maria’s leg and arm up and down with little resistance. Maria’s eyes were full of tears as she answered questions with a clear and strong voice. She said, “Thank you so much doctor. I am so glad that I can now speak very clearly again.” Several minutes later, Maria was able to move her left leg and her left arm by herself. She was able to pull and push her left leg so strongly that the doctor was encouraged to ask her if she would like to try walking. She did not hesitate and said with a clear voice, “Yes. I would like to try.” While she was walking back and forth in her room exercising her leg with the assistant helping, she kept saying, “Thank you,

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thank you so much for this miracle.” In this case, the hemiplegia was caused by cerebral hemorrhage, which has the worst prognosis for the sequelae of stroke, compared to cerebral embolism and cerebral thrombosis. After cerebral hemorrhage, the patient should get acupuncture treatment as soon as his or her condition is stable. The earlier the patient gets treatment, the better the prognosis will be.

Fibromyalgia Fibromyalgia is a chronic disorder characterized by diffuse or specific pain in muscles, ligaments, tendons, joints, or bone. Also, patients experience multiple tender points and fatigue. Fibromyalgia affects more females than males. Symptoms and signs can vary depending on stress, physical activity, weather changes, or even the time of day. Common symptoms and signs include widespread pain and stiffness, fatigue and sleep disturbances, heightened sensitivity of the skin, headache and facial pain, irritable bowel syndrome, weakness of limbs, muscle spasms, and impaired concentration and short-term memory.9 The degree of symptoms may also vary greatly from day to day with periods of flare-ups or remissions. Fibromyalgia often starts as a result of some mental or physical trauma, major surgery, or disease. Symptoms are often aggravated by unrelated illness or changes in the weather. The cause of fibromyalgia is still unknown. One theory states that patients with fibromyalgia have a lower threshold for pain because of increased sensitivity in the brain to pain signals. Other theories include abnormalities of the autonomic nervous system, changes in muscle metabolism, injury, infection, psychological stress, or hormonal changes. There is no universal cure for fibromyalgia in Western medicine. In general, treatment emphasizes minimizing the symptoms and improving general health. Scalp acupuncture has a very good track record for treating fibromyalgia. Many patients have shown significant improvements with just a few treatments in our practice. Effective areas for fibromyalgia are sensory, tremor, foot motor and sensory, and head area. For both the sensory area and tremor area, needles should be inserted bilaterally. The practitioner should choose secondary areas based on symptoms in Western medicine and patterns in Chinese medicine. A good technique is to put one needle on the Shenmen point on the ear to help patients relax and reduce the sensitivity of the needle insertion and stimulation of the scalp. Use as few needles as possible in the scalp, and rotate them at least 200 times per minute with thumb and index finger for two minutes. The doctor should twirl the needles as gently as possible in the beginning so that the patient can tolerate the intense sensations, and then gradually increase the intensity of the stimulation. Repeat stimulation every 10 minutes. During treatment, patients may have some or all of the following sensations: hot, cold, tingling, numbness, heaviness, distention, or the sensation of water or electricity moving along their spine, legs, or arms. Tell patients before the needles are inserted that these sensations are normal, and patients who experience some or all of them usually respond and improve more quickly. This lends encouragement to patients to come back for additional treatments; however, it is important to also convey to patients that if they do not have such sensations, they could still have immediate, positive results. Retain the needles in place for 25 to 30 minutes. Initially, treatment should be given two to three times per week. After a few weeks, it can be spaced out to once a week and then twice a month.

The patient should be treated about once a month thereafter, if a remarkable improvement is obtained. A therapeutic course consists of 10 treatments. It is very helpful if other acupuncture methods are added to scalp acupuncture treatments as adjunct therapies. The selection of body acupuncture points should be individualized based on the differentiation of patterns in Chinese medicine. For instance, Li-3, GB-34, and Li-14 are used for liver stagnation Qi, and Ki-3, Ki-6, and Ki-7 for deficiency of the kidneys. Cupping is another valuable method for patients with fibromyalgia. The area for cupping is around the gallbladder meridians because pains that patients with fibromyalgia normally have are located on the area that GB energy is distributed. The most frequently used points on the gallbladder meridians are GB-20, GB-21, GB-30, GB-31, GB-34, and GB-41. In late stages of fibromyalgia, the kidneys are often affected. Therefore, the points to reinforce the kidney are usually very helpful, such as Ki-3, UB-23, and GV-4. In addition, fibromyalgia often becomes worse with stress: it may be physical, emotional, or psychological. Therefore, the internal organ areas in scalp acupuncture that function to relieve anxiety, irritability, worry, or depression should be combined with the foot motor and sensory area for the best results. Case Report 5—Fibromyalgia Judy, a 48-year-old female came to our clinic in Santa Fe, New ­Mexico in the summer 2002. Judy was diagnosed with fibromyalgia in 1998. Previously, she had been a physically active young woman. She participated in many exercises and sports, such as aerobics, skiing, jogging, and hiking. For the last 10 years, these activities had to stop because the pain in her neck and back made simple tasks such as washing the dishes nearly unbearable, much less exercise. Her legs hurt so severely that even walking a short distance left her in tears. Every morning when she woke up, her neck was so stiff and painful that it was impossible for her to turn her head. The pain became progressively worse and spread through other areas of her body. She began to gain weight and feel depressed. She started to have more discomfort including insomnia, fatigue, mood swings, poor memory and concentration, and either diarrhea or constipation. Her immune system was so weak that she caught flu or colds frequently. Although she received many kinds of therapy, Judy showed little improvement. Some physicians seemed to be tired of hearing her time-consuming complaints. Examination showed that she had a red tongue with a thick white coating and teeth-marks, and her pulses were thready and wiry. Judy had a different experience during her first scalp acupuncture treatment. She felt her body totally relax and fell deeply asleep just a few minutes after the needles were inserted in her scalp. She felt completely at ease when she woke up and said as she was leaving, “I am looking forward to my next treatment.” After only six treatments, her pain and stiffness were reduced by about 70%. She woke up renewed instead of feeling as if she had not slept at all. She also no longer felt the searing pain in her neck, back, and legs that used to bring her to tears regularly. By the tenth treatment, Judy had achieved significant improvement over insomnia and fatigue. She was thrilled to start exercising again and hoped to resume many of the physical activities she had once loved. She told friends, “I cannot find the words to describe how much scalp acupuncture has changed my life.” Before scalp acupuncture, Judy had lost all hope of ever having her old health back, but after 20 treatments, Judy hardly experienced any pain . She had lower back pain occasionally but it was manageable;

The Treatment of Pain Through Chinese Scalp Acupuncture  183

and receiving scalp acupuncture treatments every 4 to 6 weeks kept the pain under control. She said she was also glad to be able to live without painkillers anymore, and did not need to rely on drugs just to get through the day. In addition to pain relief, Judy reported that her immune system was stronger than ever, and she rarely suffered from colds or flu since receiving scalp acupuncture treatments.

Restless Legs Syndrome Restless legs syndrome is a neurologic movement disorder characterized by abnormal sensations in the legs, and an uncontrollable urge to move them to relieve these unpleasant feelings. The sensations are often described as antsy, electrical creeping, itching, pins and needles, pulling, tugging, painful, or like insects were crawling inside the legs. The abnormal sensations and urge to move can occur in any part of the body; however, the most cited location is the legs. Any inactivity such as lying down or sitting can trigger those sensations and the subsequent urge to move. Movement usually brings immediate relief but it is often only temporary and partial. Most patients find that the symptoms are less noticeable during the day and more pronounced in the evening or night. The exact cause of restless legs syndrome is still unknown. Generally, it is a lifelong condition for which there is no cure in Western medicine. Scalp acupuncture has positive results with restless legs syndrome, and it usually produces immediate beneficial responses in the initial treatment. Significant and complete reduction of restless legs syndrome has occurred in approximately 85% of people receiving scalp acupuncture in our clinics. Although the norm has been that symptoms gradually disappear with each treatment, it is not uncommon for some patients to experience the symptoms worsening during their treatments. If restless legs are not well controlled by scalp acupuncture alone, patients may experience better results when combining treatment with body acupuncture. Commonly used points are Li-3, GB-34, Sp-6, and UB-18. However, for patients with severe restless legs, it is not advisable to use body points in their legs. If patients constantly move their legs while needles are inserted, this could cause severe leg pain and muscle spasm. The effective locations to insert needles for restless legs syndrome are foot motor and sensory area, tremor area, and Upper one-fifth sensory area. Foot motor and sensory and tremor areas should be inserted with needles and stimulated unilaterally. Rotate the needles at least 200 times per minute with thumb and index finger for 1 to 3 minutes. The doctor should twirl the needles as vigorously as the patient can tolerate and repeat this stimulation every ten minutes. During the treatment, some patients may feel their restless legs becoming relaxed and feel less of an urge to move them. Or some patients may experience their tremors becoming a little more severe. Those patients with some or all of these sensations usually respond and improve more quickly. However, those who do not have such sensations could still have immediate positive results. Retain the needles for 25 to 30 minutes; the treatment is given two to three times per week; and a therapeutic course consists of 10 treatments. Case Report 6— Restless Legs Syndrome Sue, a 72-year-old female, was referred to our clinic in Albuquerque, New Mexico by her primary care physician. She had suffered from restless legs syndrome for more than 15 years. Because Sue felt her legs creeping and burning, she could not keep them still

during the day or night. Her restless legs became even more pronounced at night to the point that she had to move around constantly to diminish her discomfort. She had difficulty falling asleep and staying asleep, resulting in severe fatigue and exhaustion. Her condition also caused depression, poor appetite, and constipation. She had a red tongue with a thin yellowish coating; and her pulses were thready and wiry. Sue was very calm as the doctor inserted four needles in her scalp. A few minutes after treatment began, she told the doctor that there was a warm sensation moving from her head down to her legs. After that, she was able to relax her legs and keep them still, which she had not been able to do for years. The abnormal sensations in her legs also showed some improvement, and she was able to tolerate these feelings. She was amazed to find that her legs stayed still for the entire 30 minutes of treatment, which she never could have done without scalp acupuncture. At the second treatment, Sue said she had hardly needed to get up the past several nights. She did not have to walk around at night to ease the strange sensations in her legs since the first treatment. She also stated that her sleep was better, she had more energy, and the depression was gradually improving as well. Her poor appetite and constipation were unchanged, however. Needles were inserted in stomach areas as well as other scalp areas during her second treatment. By the third treatment, Sue said, “I can sleep through the night now because my legs do not bother me anymore.” By the sixth treatment, Sue was very happy to report that she had not had any restless legs symptoms for several weeks, and her appetite and bowels had returned to normal. Sue was now sleeping well, and she was joyful that she had a lot more energy. Examination showed that her tongue had become light red with a thin white coating, and her pulses had changed to soft. She did not need further acupuncture and started to really enjoy her senior years.

Multiple Sclerosis Multiple sclerosis (MS) is a progressive disease of the central nervous system in which communication between the brain and other parts of the body is disrupted. There are multiple scars on the myelin sheaths, which comprise a fatty layer surrounding and protecting the neurons of the brain and spinal cord. Myelin allows for the smooth, high-speed transmission of electrochemical messages between the brain, the spinal cord, and the rest of the body. When myelin is destroyed or damaged, the ability of the nerves to conduct electrical impulses to and from the brain is disrupted, which causes the various symptoms of MS. Approximately 300,000 people in the United States and 2.5 million people worldwide suffer from MS. It primarily affects adults, with age of onset typically between 20 and 40 years, and is twice as common in women than in men. The effects of MS can range from relatively benign in most cases to various degrees of disability. However, the symptoms for some are devastating. Symptoms and signs of MS vary widely depending on the location of the affected myelin sheaths. Common symptoms may include numbness, tingling or weakness in one or more limbs, partial or complete loss of vision, double or blurring of vision, tremor, loss of balance and mobility, unsteady gait, fatigue, and dizziness. Some patients also might develop muscle stiffness or spasticity, paralysis, slurred speech, dysfunction of bladder or bowel, depression, and cognitive impairment. MS is unpredictable and varies in severity. In some patients it is a mild illness, but it can lead to permanent disability in others. In the worst cases, patients with MS may be unable to write, speak, or walk.

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184  Complementary and Alternative Medical Procedures

MS can occur either in discrete attacks or slowly over time. Although the functioning of systems may resolve completely between episodes, permanent neurologic problems usually persist, especially as the disease progresses. Many risk factors for MS have been identified, but no definitive cause has been found. Currently, MS does not have a cure in terms of conventional treatments but a number of therapies can be used to treat the disease symptomatically. Scalp acupuncture has been proved to have the most success in the treatment of MS and other central nervous system damage when compared to other acupuncture modalities including the ear, body, and hand. Scalp acupuncture not only can improve the symptoms, the patient’s quality of life, and slow the progression of physical disability, but also it can reduce the number of relapses. Scalp acupuncture treatment for MS has had much success in reducing numbness and pain, decreasing spasms, improving weakness and paralysis of limbs, and improving balance. Many patients also have reported that their bladder and bowel control, fatigue and overall sense of well-being significantly improved after treatment. Recent studies have shown that scalp acupuncture could be an effective modality in controlling MS. Scalp acupuncture often produces remarkable results after just a few needles are inserted.10 It usually relieves symptoms immediately, and sometimes it takes only several minutes to achieve remarkable results. Scalp acupuncture areas may be chosen according to the patient’s particular symptoms. The primary acupuncture areas for patients with motor problems such as paralysis, weakness of limbs, or abnormal sensations in limbs, including tingling, numbness or pain, are the motor area and the sensory and foot-motor areas. Those areas should be inserted with needles and stimulated unilaterally or bilaterally, according to the patient’s manifestations. Select the balance area or dizziness area of the scalp, respectively, depending on which symptom the patient manifests. The tremor area of the head should be chosen if patients have limb spasm. Many patients had a quick positive response in controlling urine and bowel functions when the foot-motor and sensory areas are stimulated. Rotate the needles at least 200 times per minute with the thumb and index finger for 1 to 3 minutes. The needles should be twirled as vigorously as the patient can tolerate and repeated every 10 minutes. During treatment, some patients may have some or all of the following sensations: hot, cold, tingling, numbness, heaviness or distention, or the sensation of water or electricity moving along the spine, legs, or arms. Those patients with some or all of these sensations usually respond and improve more quickly. However, those who do not have such sensations still could have immediate positive results. Keep the needles inserted for 30 to 45 minutes. The treatment should be administered two to three times per week and a therapeutic course consists of 10 treatments. There are many different acupuncture techniques to treat MS. Although scalp acupuncture has the fastest track record for improving symptoms, other techniques are also necessary for further improvement. Regular body acupuncture, electric acupuncture, and moxibustion, as well as physical therapy and massage, can combine with scalp acupuncture to speed the time of recovery. Case Report 7—Burning and Stabbing Pain A 52-year-old female received scalp acupuncture treatment at National Healthcare Center in Albuquerque, New Mexico. After the first symptoms occurred in January 2007, the patient was finally diagnosed with MS in in August of that year. Although various types

of medications were provided, she experienced little improvement. The patient described severe burning and stabbing pain throughout her whole body that interrupted her sleep and caused loss of emotional control. She also had occipital headaches and loss of balance that made her unable to walk or turn around. The examination revealed that she could not stand still if her eyes were closed; and she could not turn around, stand on one leg, or walk from toe to heel. The movements of touching her nose and touching both index fingers together were accomplished slowly and only with great effort. Her tongue was red and somewhat purple, with a thin white coating. The pulse was wiry and thready. As soon as she underwent scalp acupuncture treatment, she started to feel the sensations of energy moving down her lower back, followed by heat sensations in her feet. Three minutes later, the burning and stabbing pain diminished considerably. She felt only some of those sensations in her right hip and abdominal area. After 12 minutes had passed, the sensation of burning and stabbing in her entire body had disappeared almost completely, except for some mild sensations in her abdomen. The patient was so excited to feel such dramatic results that she could not wait to test her movements. She was very surprised to find that she had no problem standing with her eyes closed, standing on either leg with the other one raised, walking in a straight line, and turning around without loss of balance. Also, she could now touch her nose and touch her index fingers together like a normal person. By the end of the treatment, her occipital headache had disappeared as well. This patient was happy to tell other MS patients that she felt like a “normal” person physically and emotionally after only one scalp acupuncture treatment. Case Report 8— Paralysis A 55-year-old female in a wheelchair received scalp acupuncture treatment. After the first symptoms occurred in 1990, the patient finally was diagnosed with MS in 2002. Both of her legs had started to become weak and heavy in the 1990s. Within 3 years, she was almost paralyzed and finally could not walk at all. The examination revealed she could not stand up straight due to the weakness in her legs, and she was unable to lift her right foot, so she had to drag it behind her when walking. Her tongue was red with a thin white coating; and her pulses were thready and wiry, with weak pulses in the kidney positions. After four needles were inserted in her scalp, the patient experienced some tingling and electrical sensations in both of her legs. Five minutes later, she felt the urge to move both legs. After exercising her legs by bending and extending them, she was able to stand up straight and walk, free to lift both her feet almost normally. Although it took a lot of effort, she was amazed to be able to walk. At first she needed two people to assist her, then only one person, and finally she was able to walk by herself. Case Report 9—Dizziness and Vertigo A 60-year-old female received scalp acupuncture treatment. After the first symptoms occurred at age 20, the patient was finally diagnosed with MS in 1994. Her major symptoms were dizziness and vertigo accompanied by temple headaches that gradually became worse over the next 7 years. Sometimes her vertigo was so severe that she felt as if the whole room was spinning violently, which caused her to fall down easily even when she was just standing. Her quality of life was completely diminished and she had to spend whole days flat on her back with her eyes closed to avoid any movement of her head. The onset of dizziness and vertigo were

The Treatment of Pain Through Chinese Scalp Acupuncture  185

exacerbated whenever she changed her position in bed or even slightly moved her head. A few years before, the patient had received more than 15 acupuncture treatments from various doctors but experienced little improvement. On examination, it was found that her tongue was red with a thick white coating and she had wiry and thready pulses. After two needles were inserted in each temple, the patient reported that she felt some weird sensations in her head that she did not know how to describe. As the doctor stimulated the needles in her head, she was able to explain that it felt like a curtain in front of her eyes had opened. These sensations made her mind clear and her temple headache disappeared. Soon after, her vertigo and dizziness diminished significantly. She moved her head upward, downward, to the left and to the right, testing whether her dizziness and vertigo really were gone. Finally, she announced, “I believe I do not have any dizziness and vertigo anymore. And this was only my first scalp acupuncture treatment!” Although MS still is an incurable disease of the central nervous system, scalp acupuncture provides an important alternative treatment approach for improving many MS symptoms and the patient’s quality of life. It slows or reverses the progression of physical disability and reduces the number of relapses. By directly stimulating affected areas of the central nervous system, scalp acupuncture has shown more effective results compared to other acupuncture techniques. Our treatments showed that many patients had instant improvements after only one scalp acupuncture treatment. The treatments also demonstrated that scalp acupuncture for MS is accessible and safe; it appears to be effective with few side effects. Scalp acupuncture not only benefits patients with MS, but also significantly helps us to better understand the mechanisms that cause the condition. It may guide us to the discovery of new effective treatments and hopefully to a cure for this disease.

Conclusion Chinese Scalp Acupuncture has been proved to be effective, safe, and inexpensive for central nervous system disorders. This is based on 37 years of empirical evidence and study in China. Many more people in the United States are seeking acupuncture treatment to alleviate their pain. Therefore, it is increasingly helpful for acupuncturists, physician acupuncturists, and Doctors of Oriental Medicine to have a working understanding of scalp acupuncture and its clinical application. Although there have been many hypotheses and research reports on scalp acupuncture for rehabilitation of paralysis and pain management in the Western medical literature over the past 38 years, there is still a long way to go in uncovering the mystery of the mechanisms of scalp acupuncture.

Drs. Jason Jishun Hao and Linda Lingzhi Hao have been teaching, researching, and practicing scalp acupuncture for 28 years. They studied with and were tutored by many famous professors, including Jiao Shunfa, the founder of scalp acupuncture, Shun Shentian and Yu Zhishun—all outstanding professors and researchers on scalp acupuncture in China for many years. Their successful cases of using scalp acupuncture have been reported in several newspapers and journals including “Stripe” published by Walter Reed Army Medical Center, “The New Mexican,” “Albuquerque Journal,” “Acupuncture Today,” “China News of Traditional Chinese Medicine,” and “Alternative Therapist.” The authors hope that acupuncture practitioners, teachers, and students will benefit from the knowledge and experience imparted in this chapter. It is intended to serve as the basis for further teaching, practice, and research. For more detailed information on scalp acupuncture please see the authors’ new book, Chinese Scalp Acupuncture, that will be published on November 2011 by Blue Poppy Press in Boulder, Colorado. They can be contacted by visiting their website www.scalpacumaster.com or call their clinic in Albuquerque, New Mexico at 505-822-9878. REFERENCES   1. Jiao Shunfa. Head Acupuncture. Bejiing: Forign Languages Press; 1993:17-22.   2. Frank Lampe, Suzanne Snyder, Jason Hao. “DOM: Pioneering The Use of Scalp Acupuncture to Transform Healing”. Alternative Therapies. MAR/APR. 2009;15(2):62-71.   3. McMillan Brett B. “Easing the Pain, Acupuncture Program Looks to help Relieve Discomfort of Troops”. Stripe. February 17, 2006:1.   4. John O’Connor, Dan Bensky. Acupuncture A Comprehensive Text. Seattle: Eastland Press; 1981:498-501.   5. Hal Blumenfeld. Neuroanatomy Through Clinical Cases. Sunderland, Massachusetts: Sinauer Associates, Inc; 2002:28-29.   6. Van Heertum Ranalk L, Tikofsky Ronald S. Functional Cerebral SPECT and PET Imaging. 3rd ed. Philadelphia, PA: Lippincott William & Wilkins; 2000:62–63.   7. Orhan Arslan. Neuroanatomical Basis of Clinical Neurology. New York: The Parthenon Publishing Group Inc; 2001:335.   8. Jason Hao, Linda Hao. “Treatment of Phantom Pain by Scalp acupuncture”. Acupuncture Today. September, 2006;7(9):10-11.   9. Shi Lingzhi, Hao Jishun. Treatment of Fibromyalgia by Eightneedle Penetrating Techniques”. Chinese Journal of Information on Traditional Chinese Medicine. Feb 2005;12(2):64. 10. Jason Hao, Linda Hao. “Treatment of Multiple Sclerosis By Scalp Acupuncture. Acupuncture Today. April 2008;9(4):12-13.

19

Herbal and Nutritional Supplements for Painful Conditions

20

Andrea H. Zengion, ND, MSAOM, and Eric Yarnell, ND Herbs and supplements are widely used by patients in pain.1 Throughout this chapter, mechanisms of action and efficacy, dosing, and safety information will be provided for each herb, supplement, and natural product for the pain syndromes for which research literature supports their use. For herbs, the medicinal portion of the plant will also be given because different parts of a plant may have different constituents and clinical effects. This chapter is meant to provide an overview, and practitioners not already trained in natural medicine should seek additional education to become proficient in the use of natural products. Natural substances offer many potential benefits for helping treat patients with pain. First, they often have long histories of use (thousands of years in some cases; the Ebers Papyrus, arguably the oldest book in the world, consists of a materia medica of traditional Egyptian medicine2), and one could argue these substances are among the best tested and most “evidence-based” medicines available.3 Second, they are largely nontoxic, although there are exceptions.4 One study found that over a 10-year period, only two deaths in the United States could be linked to herbal medicines.5 Third, they are often cost effective, again, with exceptions. Finally, they act on multiple pathways, some of which are not addressed by any other existing therapies.6 Study of the mechanism of action of some natural treatments has led to breakthroughs in the understanding of pain pathophysiology and to the development of entirely new categories of medications. For example, investigation of capsaicin brought about enhanced understanding of vanilloid receptors, TRPV1, unmyelinated C fibers, substance P, and novel topical treatments for pain syndromes.7

given a near total lack of comparative studies, but such extracts do satisfy the demand for uniformity, simplicity, and patentability prevalent in a market-driven health care system and society.12 Throughout this chapter, both refined and crude herbal extracts will be listed for completeness, although often it is unknown which form is superior (Table 20-1).

Chinese Herbal Medicine: Ancient and Modern Chinese medicine is one of the most ancient healing systems on the planet.13,14 Based on a distinctive physiology quite unlike Western medicine, it is still in use today. Herbs play a central role in Chinese medicine, although acupuncture is more widely accepted in Western society. Unlike in Western cultures, herbs in traditional Chinese medicine are almost always given in complex formulas,15 as it was observed that combining herbs produces a stronger, more specific therapeutic effect, and that herbs used together mitigate some of the adverse effects they may engender as single entities. Formulation is still the most common way to prescribe Chinese herbs.16 Nevertheless, biochemical and pharmaceutical research techniques have been extensively applied to Chinese herbs, and now singleherb medicines or isolated constituents extracted from single herbs are used more widely. Caution is warranted with these much more recent innovations, and the traditional formulas are preferred in most cases. Many of these same arguments could be made about traditional medicine systems from around the world, such as Ayurveda and Unani-Tibb in South Asia, or Native ­American medicine.

Antiinflammatory Herbal Medicines

Western Herbal Medicine: Complexity and Synergy Herbs have been an important part of Western medicine for thousands of years.8,9 Herbs contain hundreds of different compounds, and traditional medicine theorizes that the constituents of medicinal plants act synergistically.10 Many studies support that complex herbal extracts often have effects that are distinct and/or greater than those of their single isolated constituents.11 In some cases, isolated compounds or highly refined extracts with just a few constituents such as silymarin, a complex of three flavonoligans from Silybum marianum (milk thistle) seed, or curcumin, a mixture of three resinous polyphenols from Curcuma longa (turmeric) rhizome, are used clinically. It is not clear if these offer advantages over more complex, less concentrated extracts,

Curcuma Longa (Turmeric) The rhizome of Curcuma longa is ground or tinctured (1:2 ratio, >45% ethanol content)6 to make medicine. Most supplements use curcumin, a mixture of lipophilic polyphenolic compounds including diferuloylmethane, demethoxycurcumin and bisdemethoxycurcumin found in the rhizome. It is traditionally used for pain and has been shown to modulate inflammatory cytokines including IL-1β, IL-12, IL-6, TNF-α, and IFN-γ.17 Osteoarthritis: In the treatment of knee osteoarthritis pain, the efficacy and safety of Curcuma were found to be comparable to those of ibuprofen.18 Rheumatoid arthritis: Curcumin inhibited proliferation of, and induced apoptosis in, the synovial fibroblasts of rheumatoid arthritis (RA) patients in vitro.19 187

Name

Indications

Dosages

Cautions

Contraindications Doses greater than 15 g per day in patients who take anticoagulants; biliary obstruction

Antiinflammatory herbs and supplements Curcuma longa (Turmeric)

Osteoarthritis Rheumatoid arthritis

1-3 g powdered tuber three times per day, or 1-3 mL  liquid extract five times per day; 500-2000 mg curcumin tid

Turmeric (but not curcumin) contains oxalates and should be taken with high-fiber or high-calcium foods to avoid exacerbation of kidney stones

Bromelain

General inflammation Exercise recovery Osteoarthritic pain Wound healing

500-2000 mg three or more times per day (potency of 2400 mcu or 3200 gdu per 1000 mg) Must not be taken with food

Because bromelain inhibits synthesis of fibrinogen and increases fibrinolytic activity, it theoretically increases the risk of bleeding

Omega-3 oils

Antiinflammatory Exercise tolerance Rheumatoid arthritis Osteoarthritis

6-9 g fish oil providing a minimum of 1.8 g EPA per day. At least 3 months of treatment is usually required for a therapeutic effect

May cause bruising in some individuals Data are varied whether omega-3 fatty acids inhibit clot formation

Some sources give a contraindication for omega-3 fats presurgically because of their possible anticoagulant effects

Angelica sinensis (Dang gui, tang kui)

General pain Dysmenorrhea

4.5-15 g dried root per day in divided doses

In traditional Chinese medicine, it is used after the first trimester of pregnancy, although its use in pregnancy is contraindicated altogether in some other sources

During pregnancy with a history of habitual miscarriage Traditionally not used in cases of diarrhea or acute viral infection In one study, Angelica potentiated anticoagulant effects of warfarin Theoretically, it may interact with other anticoagulants as well

Zingiber officinalis (Ginger)

Inflammatory pain Migraine Dysmenorrhea Osteoarthritis Rheumatoid arthritis Myalgia

250 mg/1 g encapsulated, one to four times per day; eaten with food as tolerated

Harpagophytum procumbens (Devil’s claw)

Low back pain

Standardized extract providing 50-100 mg harpagosides per day Tincture (1:2-1:5): 4-5 mL three times per day Liquid extract (1:1): 3-4 mL three times daily

Harpagophytum may potentiate effects of warfarin

Contraindicated in hyperchlorhydria, acute peptic ulcers, and acute diarrhea

Boswellia serrata ­(Frankincense)

Osteoarthritis Collagenous colitis

150-400 mg boswellic acid taken three times daily

Caution: may cause contact dermatitis or mild diarrhea or urticaria

Tanacetum parthenium (Feverfew)

Migraine

25-225 mg per day Tincture (1:2 or 1:3) 3-5 mL three times per day for prevention and up to 10-12 mL five times a day for acute treatment Patients may chew 1-3 fresh leaves daily for migraine prophylaxis, although mouth ulcers are occasionally reported with this administration

Caution in allergy to members of the Asteraceae (Compositae), and during pregnancy because it may stimulate uterine contraction

Centrally-acting analgesics Corydalis yanhusuo (Yanhusuo)

General pain Cancer pain Dysmenorrhea

Crude herb, decocted: 4.5-12 g per day, divided doses Tincture: 0.25-1 mL three times daily

In Chinese medicine, this herb is generally  contraindicated during pregnancy

188  Complementary and Alternative Medical Procedures

Table 20-1  Summary of Herbs and Supplements Used for Treatment of Pain

Cannabis sativa (Marijuana)

Postsurgical pain Neuropathic pain Sleep improvement Rheumatoid arthritis Severe pain/adjunct to opiate treatment

Further study is needed to determine dosage for most conditions A therapeutic window should be established because Cannabis may cause hyperalgesia at high doses

May worsen hepatic fibrosis in patients with Hepatitis C

Hypericum perforatum (St. John’s Wort)

Otitis media Burning mouth syndrome Neuropathy

Tincture (1:5): 2-4 mL three times per day Decoction: 2-4 g dried herb taken three times per day Standardized extract: 300 mg tid providing 0.3% hypericin and 5% hyperforin

Due to its upregulatory effects on some cytochrome P450 enzymes Hypericum reduces serum levels of certain drugs Drugs for which interaction has been  demonstrated include anti-HIV protease  inhibitors, cyclosporine, atorvastatin,  simvastatin, finasteride, and digoxin It may also decrease efficacy of oral  contraceptives At extremely high doses, Hypericum may cause photosensitivity in light-skinned individuals

Use of Cannabis, especially in adolescents and people at risk for mental illness, may be related to onset of psychological diseases such as psychosis or schizophrenia

(1:10) one drop in approximately 120 mL three times daily

Bryonia alba (White bryony) Topicals Postherpetic  neuralgia Diabetic neuropathy Arthritis Mouth pain following chemotherapy and radiation Postmastectomy pain Trigeminal neuralgia Cluster headaches

Typically requires application two or three times a day or pain sensation may return

Capsaicin causes topical irritation (usually minor) on initial application, but this almost always passes with frequent use To achieve a therapeutic effect, patients must often overcome an initial period of discomfort before desensitization has occurred

Urtica dioica (Stinging nettle)

Joint pain

Apply fresh leaf topically to affected area for approximately 30 seconds two or three times. Repeat as needed

Theoretically, internal use may decrease efficacy of warfarin due to nettle leaf’s substantial vitamin K content

Symphytum officinale (Comfrey)

Osteoarthritis Back pain

1-2 g topically three to five times per day

uPA-containing extracts pose a minor risk of hepatotoxicity and carcinogenicity, although these alkaloids show only minimal transdermal absorbtion uPA-free extracts pose no such risk

Arnica montana

Bruising Osteoarthritis

Apply topically three to five times per day

Not to be taken internally or applied to broken skin or near the mouth Homeopathic topical preparations do not pose risk of toxicity in pregnancy

Dimethyl sulfoxide (DMSO)

As a carrier for other analgesics CRPS

Applied topically five times per day

May cause skin irritation

Contraindicated in pregnancy in physiologic doses

Continued

Herbal and Nutritional Supplements for Painful Conditions  189

Capsicum frutescens (Cayenne)

20

Name

Indications

Dosages

Cautions

Echinacea spp. (Purple coneflower)

Pharyngeal pain

Throat spray: Two puffs every two hours for duration of symptoms Tincture: 1-5 mL in water as a gargle

Contraindication in allergy to members of the Asteraceae (Compositae) family

Contraindications

Salicylate-containing herbal medicines Salix alba (White willow)

Low back pain Osteoarthritis

Standardized extract providing 120-240 mg salicylate Fluid extract (1:1): 2-4 mL three times daily Fluid extract (1:2): 3-5 mL three to five times per day

Salicylate allergy

Hypnotic analgesics Valeriana officinalis (Valerian)

Extract 1:2-1:3: 3-5 mL three times daily with  5-10 mL at bedtime

Occasionally, Valeriana may cause agitation

Piscidia spp. (Jamaican dogwood)

Crude root bark (dried): 2-4 g three times daily Aqueous extract: (1:2) 1-2 mL three times per day Tincture: (1:5) 5-15 mL three times per day

Dosing simultaneously with other sedative therapies because Piscidia may amplify these effects

Eschscholtzia californica (California poppy)

Tincture (1:2): 1-2 mL three times per day

Pregnancy, bradycardia and cardiac insufficiency

Contraindicated in pregnancy; animal studies indicate that cryptopine causes uterine  stimulation

Nutritional cofactors Methylsulfonylmethane (MSM)

Arthritides

1000-3000 mg three times per day

None

Riboflavin

Migraine

400 mg per day

Lipoic acid/alpha lipoic acid/thioctic acid

Migraine prophylaxis Diabetic neuropathy

600-1800 mg orally per day in divided doses 600 mg daily intravenously

May worsen paresthesias when treatment first begun May decrease blood glucose levels

S-adenosyl methionine  (SAM-e)

Osteoarthritis Fibromyalgia

800-1600 mg per day

Rare episodes of mania and hypomania have been reported in depressed patients taking SAM-e Drug-herb interactions may occur with ­concurrent administration of serotonergic drugs, levodopa or monoamine oxidase inhibitors

Glucosamine sulfate, chondroitin sulfate

Osteoarthritis

1500 mg glucosamine sulfate per day 400-1200 mg chondroitin sulfate per day

Magnesium

Pediatric migraine Muscle cramps Dysmenorrhea

Children: 9 mg/kg/day Adults: 250-600 mg per day

Magnesium citrate supplements can have an osmotic laxative effect at high doses This effect may be seen to a lesser degree in other forms

None

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Table 20-1  Summary of Herbs and Supplements Used for Treatment of Pain—cont’d

Hormones Melatonin

Migraines Headaches Postoperative  analgesia

1-20 mg, generally taken only at bedtime or just before a painful procedure

May cause daytime grogginess and delayed recovery from anesthesia

Vitamin D

Osteomalacia Diabetic neuropathy Low back pain Rheumatoid arthritis Statin-induced myalgia Migraine Multiple sclerosis

1000-10,000 IU per day; doses of 50,000 IU are also frequently given for several weeks at a time

Calcium oxalate nephrolithiasis

Coenzyme Q10 (CoQ10)

Migraines Chronic fatigue syndrome

Pediatric: 1-3 mg/kg/day Adults: 150 mg/day with food

Antagonizes warfarin and other anticoagulants, may increase effect of hypotensives

Hypercalcemia, hyperphosphatemia, vitamin D toxicity, sarcoidosis

Miscellaneous substances Migraines  Raynaud phenomenon/disease

Standardized extract: 120-240 mg per day, in divided doses

Ginkgo should be discontinued at least 36 hours prior to surgery It may interact additively with other anticoagulants Drug-herb interactions are possible with a number of other pharmaceuticals, including anticonvulsants, antidepressants, cyclosporine and thiazide diuretics

Centella asiatica

Venous insufficiency

180 mg per day of total triterpenic fraction

Caution in patients with cholestasis, celiac disease, fat malabsorption disorders, and deficiency of fat-soluble vitamins due to high saponin content of Centella

Viburnum opulus (Cramp bark), Viburnum prunifolium (Black haw)

Dysmenorrhea

V. opulus: Tincture: 5-10 mL (1:5) three times per day Encapsulated or decocted crude herb: 2-4 g three times per day V. prunifolium: Tincture: 5-10 mL (1:5) three times per day Encapsulated or decocted: 2.5-5 g three times per day

V. prunifolium is also used to treat hypertension; use caution in hypotensive patients This herb also contains oxalates and is generally given in doses too low to warrant caution in patients with calcium oxalate nephrolithiasis

Scutellaria laterifolia (Skullcap), Scutellaria baicalensis (Huang Qin)

Osteoarthritis

Dried herb: 1-2 g three times per day Liquid extract (1:2): 0.6-1.5 mL three times per day Tincture (1:5): 1-2 mL three times per day

Not to be used for extended periods during pregnancy

None

Rosa canina

Osteoarthritis

4-5 g powder twice daily

None currently known

None currently known

Solidago chilensis (Brazilian arnica)

Low back pain

10 g gel applied topically twice daily

Herbal and Nutritional Supplements for Painful Conditions  191

Ginkgo biloba

Allergy to members of the Asteraceae family

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192  Complementary and Alternative Medical Procedures

Dosage: 1 to 10 g powdered rhizome three to five times per day or tincture (1:1 or 1:2) 3 to 10 mL three to five times per day. 500 to 2000 mg curcumin three to five times per day. Cautions/contraindications: Patients on anticoagulant therapies should not be given doses of Curcuma longa in excess of 15 g per day. Turmeric (but not curcumin extracts) contains large quantities of oxalate and should be taken with high-fiber and high-calcium foods to avoid exacerbation of kidney stones.20 Per German Commission E monographs, it should not be given in cases of biliary obstruction.21 Bromelain Bromelain is a mixture of enzymes derived from pineapple. Its effects are mainly a product of its proteolytic activity, which stimulates fibrinolysis by increasing plasmin, but bromelain also has been shown to prevent kinin production and to inhibit platelet aggregation.22 Because its mechanism of action is generally antiinflammatory, rather than specific to a particular disease process, bromelain is used to treat a variety of pain and inflammatory conditions. When given to treat pain, it must be administered away from food because it will act as a digestive enzyme if consumed with food. Sports medicine: A study examining the effects of a mixture of proteases, including bromelain, after downhill running concluded that these enzymes improved post-workout recovery of contractile function and attenuated duration of muscle soreness compared to placebo.23 Another study comparing placebo to ibuprofen and to bromelain in a trial of eccentric exercise (weightlifting) found that neither ibuprofen nor bromelain improved delayed onset muscle pain (elbow flexor soreness), range of motion or concentric peak torque compared to placebo.24 Arthritic and knee pain: Bromelain improves functionality and decreased pain in mild acute knee pain and knee osteoarthritis.25 In one study, efficacy of treatment with a bromelain-rutosidetrypsin product compared favorably to treatment with diclo­ fenac.26 A review article found bromelain effective for treatment of knee and shoulder osteoarthritis, but reported varying degrees of patient tolerance to high doses. Adverse effects included diarrhea, flatulence, nausea, dry mouth, unspecified allergic reaction, and skin irritation.27 Wound healing: Bromelain may be useful postsurgically to shorten healing time and to reduce levels of edema, pain, and ecchymoses.28 Dosage: 500-2000 mg three or more times per day (potency of 2400 mcu or 3200 gelatin dissolving units (gdu) per 1000 mg) away from food. Cautions/contraindications: Animal studies indicate that bromelain inhibits fibrinogen synthesis and increases fibrinolytic activity.29 Although bromelain has not been shown to increase risk of bleeding, this result is theoretically possible. Omega-3 Oils Omega-3 essential fatty acids are used by the body to form cell membranes and antiinflammatory prostaglandins, among other important molecules. Murine studies indicate that these fats produce resolvins and protectins, novel lipids with antiinflammatory properties. Although these fatty acids do not act specifically on nociceptive pathways, their administration has the well-­documented effect of reducing inflammation in the body.30 Fish oils are a major source of omega-3 fatty acid supplementation, especially of eicosapentaenoic acid (EPA) and docosahexaenoic

acid (DHA), which are direct precursors of series three prostaglandins. Flax oil also contains a high proportion of α-linolenic acid, which is itself a precursor to DHA and EPA, but requires enzymatic conversion before having a direct antiinflammatory effect and is, therefore, less efficient for this purpose. Because of this, DHA and EPA have stronger and more direct antiinflammatory effects. A study comparing two marine oils (seal and cod liver oils) found no difference in their efficacy,31 suggesting that the origin of the fatty acids is less important than their EPA/DHA content. Fatty acid source is a concern with regard to heavy metal and PCB content of the supplements, and only products that employ third-party verification of purity should be given. Exercise tolerance: A study examining post-exercise pain in men who were not part of a regular training program found that administration of omega-3 fatty acids reduced pain and improved range of motion 48 hours after exercise.32 Myocardial and skeletal muscle membranes take up omega-3 fatty acids at a higher rate than other organs. A study of fish oil administration showed that this incorporation results in decreased myocardial oxygen consumption with the same degree of performance; lower resting heart rate; and decreased episodes of arrhythmias. In skeletal muscle, fish oil administration resulted in increased insulin sensitivity and efficiency.33 Arthritides: A Cochrane meta-analysis of patients with rheumatoid arthritis or joint pain secondary to dysmenorrhea or inflammatory bowel disease found significant reduction in patient-reported pain, NSAID consumption and number of painful joints. The authors concluded that benefit is likely for osteoarthritis patients as well, although clinical trials are still needed.30 Dosage: 6 to 9 g fish oil providing 1.8 g EPA per day minimum. At least 3 months of treatment is usually required to see therapeutic effect. Caution/contraindication: Caution: May cause bruising in some individuals. Data are varied as to whether or not omega-3 fatty acids inhibit clot formation. One study found that omega-3 acids potentiate the effects of dual antiplatelet therapy (aspirin and clopidogrel).34 A placebo-controlled study examining interactions between omega-3s and warfarin found that 3 to 6 g of fish oil given daily did not produce a statistically significant difference in PT-INR.35 Contraindication: Some sources give a contraindication for omega-3 fats presurgically because of their possible anticoagulant effects. Angelica sinensis (Dang Gui, Tang Kui, Dong Kuai) The root is used as medicine and the herb is tinctured, decocted, or powdered and encapsulated. In China, it is also injected locally into areas of low back and postsurgical pain with significant improvement of symptoms.36 Angelica is commonly used in Chinese medicine for gynecologic complaints, including dysmenorrhea. Active constituents include ligustilide, which has been demonstrated in murine studies to be antinociceptive and antiinflammatory.37 General pain: A controlled clinical trial found that Angelica improved pain and intensity during cold pressor testing.38 Dysmenorrhea: Aqueous and ethanol extracts of Angelica tend to stimulate the uterus, whereas the essential oil inhibits its contraction. Interestingly, studies have shown that administering the herb to a contracted uterus results in relaxation, whereas

Herbal and Nutritional Supplements for Painful Conditions  193

administering it while the uterus is relaxed results in contraction. In traditional Chinese medicine, decoction is the most common mode of administration, but a study in which the essential oil was given reported a 76% reduction in dysmenorrhea.36 Dosage: 4.5 to 15 g dried root per day in divided doses. Caution/contraindications: Contraindications: Should not be given during pregnancy in women with a history of miscarriage. Traditionally not used in cases of diarrhea or acute viral infection. In one study, Angelica potentiated warfarin’s anticoagulant effects, although the herb does not affect prothrombin time when given alone (and thus may have worked by inhibiting platelet aggregation). Because of these findings, it is theorized that Angelica may interact with other anticoagulants as well.36 In traditional Chinese medicine, it is used after the first trimester of pregnancy, although its use in pregnancy is contraindicated altogether in other sources. Zingiber officinalis (Ginger) The rhizome of Zingiber has been used in traditional Asian medicines, including Chinese and Ayurvedic herbalism, for millennia. Today, it is administered as encapsulated powder, in decoction, food, or tincture. Ginger is more commonly used for treatment of digestive complaints than it is for pain, but has been shown to inhibit prostaglandin and thromboxane formation in platelets39 and serotonin receptors in vivo. In vitro studies of human synoviocytes have demonstrated that Zingiber extract inhibits TNF-α activation and cyclooxygenase-2 expression.40 Migraines: A product which combined Tanacetum and Zingiber demonstrated effect in aborting incipient migraine when treatment was administered in the headache’s early phases. Results were promising, although the study was of small size.41 No definitive studies have yet been performed, but evidence suggests that Zingiber may be effective in migraine prophylaxis.39 Dysmenorrhea: A double-blind clinical trial found Zingiber to be as effective as ibuprofen in treating pain and reducing severity of dysmenorrhea.42 Arthritides: Study data are mixed, with one showing reduction of symptoms of knee osteoarthritis and another crossover study showing symptomatic improvement of osteoarthritis only before crossover. Some relief of pain and swelling was reported in a retrospective case analysis of rheumatoid arthritis, osteoarthritis, and myalgia patients.40 Dosage: 250 mg-1 g encapsulated, one to four times per day; tincture (1:3 to 1:5) 1 to 5 mL one to four times per day; eaten with food as tolerated. Caution/contraindications: Caution in gastric diseases such as peptic ulceration, doses of less than 4 g per day in persons on anticoagulant therapies or with risk of hemorrhage. There is a theoretical concern that Zingiber may inhibit clotting, but relatively little data supporting that assertion. One study found that administration of moderate doses (3.6 g powdered rhizome extract per) did not alter PT-INR.43 Another study demonstrated that one 10 g dose of powdered rhizome resulted in decreased platelet aggregation in patients with coronary artery disease.44 A second study found that Zingiber counteracted the antifibrinolytic properties of fatty meals and even increased fibrinolysis.45 Other studies, however, including one in which subjects consumed 15 g of fresh rhizome or 40 g of cooked stem, found no antiplatelet activity in vitro.46

Harpagophytum procumbens (Devil’s Claw) This herb is native to southern Africa, and it grows in a fairly limited distribution, making it somewhat threatened in the wild. Because of this, only cultivated material should be purchased. The tuber is used therapeutically, and active constituents appear to be iridoid glycosides including harpagosides. This herb is usually administered as an aqueous or alcohol extract. Mechanism of action is unknown, but appears to be mediated via the central nervous system with possible peripheral antinociceptive effects. A rodent study found that its effects were attenuated by naloxone administration, suggesting that it acts at least in part via opioidergic pathways.47 Low back pain: Two studies provided strong evidence that a dose of 50 mg harpagosides per aqueous administration provides short-term relief for low back pain. Another provided moderate evidence that 100 mg harpagosides per aqueous dose effectively reduces low back pain in the long term. Furthermore, 60 mg harpagosides taken daily for short-term treatment of chronic low back pain was as effective as 12.5 mg rofecoxib.48 Dosage: Standardized extract providing 50 to 100 mg harpagosides per day. Tincture (1:2-1:5): 4 to 5 mL three times per day. Liquid extract (1:1): 3 to 4 mL three times daily. Caution/contraindication: Contraindicated in hyperchlorhydria, acute peptic ulcers, and acute diarrhea. Harpagophytum may potentiate warfarin.21 Boswellia serrata (Frankincense) Boswellia acts as an antiinflammatory by its inhibition of 5-lipoxygenase, although it has no apparent effect on cyclooxygenase. Because it is a resin, it is relatively hydrophobic and must be tinctured by using a menstruum with high ethanol content. In Chinese herbal medicine, Boswellia carterii, a similar species, is an important herb for treatment of pain and healing of ulcers and is often paired with myrrh. Extracts may be standardized to 37.5% to 65% boswellic acids (considered to be the active constituents), although it may also be taken as crude herb in pill or capsule form, or, in Chinese herbal medicine, used topically or added in small amounts to decoctions of other herbs. Adverse effects may include gastrointestinal symptoms because tannins are sometimes difficult to digest. Osteoarthritis: B. serrata increases joint flexion and reduces pain in knee osteoarthritis. Compared to valdecoxib, Boswellia’s therapeutic activity had a slower onset but persisted longer (valdecoxib’s effects did not persist after cessation of therapy, whereas the Boswellia group maintained improvement up to 1 month after cessation). Boswellia administration resulted in statistically significant improvement of pain, stiffness, and ability to perform daily activities.49 A double-blind, placebo-controlled clinical trial for 5-loxin, a Boswellia extract enriched with 30% 3-O-acetyl-11-ketobeta-boswellic acid (AKBA) found that, administration of the drug resulted in statistically significant reduction of pain, improvement of functional ability, and reduction in levels of matrix metalloproteinase-3 in synovial fluid. Diarrhea, abdominal pain, nausea, mild fever, and weakness were reported as adverse effects.50 Collagenous colitis: A small study demonstrated greater clinical remission rate with administration of Boswellia extract than with placebo after 6 weeks of treatment.51 Dosage: 150 to 400 mg boswellic acid taken three times daily. Caution/contraindications: Caution: may cause contact dermatitis or mild diarrhea or urticaria.21

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194  Complementary and Alternative Medical Procedures

Tanacetum parthenium (Feverfew) The leaf is typically used as medicine and is eaten fresh or taken as tea, encapsulated crude herb or tincture. It appears to act by inhibiting formation of prostaglandins in the arachidonic acid pathway, inhibiting serotonin and histamine secretion, preventing platelet aggregation, or by reducing vascular response to vasoactive amines. Parthenolide is supposedly one of the major active constituents and appears to inhibit arachidonic acid release, but studies using parthenolide alone do not yield the clinical results obtained by administration of the whole herb.52 Migraine: Feverfew has been shown to decrease frequency and severity of migraines when used as a prophylactic, including in a double-blind, randomized, controlled trial.53 A study that used a high-percentage (90%) ethanol extraction did not demonstrate efficacy against migraines, suggesting that such a high proportion of ethanol does not adequately extract the constituents necessary for therapeutic effect. As a consequence, crude herb, aqueous extracts or extracts with an ethanol content below 90% are more likely to have positive clinical effect.6 Additionally, like many pharmaceutical treatments for migraines, patients sometimes present with rebound migraine, sleep symptoms, and anxiety after withdrawal from long-term T. parthenium use.52 Although most studies examine Tanacetum’s use as a migraine prophylactic, a small study demonstrated that product containing Tanacetum and Zingiber demonstrated effect in aborting incipient migraine when treatment was administered in the headache’s early phases.52 Dosage: 25 to 225 mg per day. Tincture (1:2 or 1:3) 3 to 5 mL three times per day for prevention and up to 10 to 12 mL five times a day for acute treatment. Patients may chew one to three fresh leaves daily for migraine prophylaxis, although mouth ulcers are occasionally reported with this administration. Caution/contraindications: Caution in allergy to members of the Asteraceae (Compositae) and during pregnancy because it may stimulate uterine contraction.52

Centrally-Acting Herbs and Supplements Corydalis yanhusuo A member of the poppy family, Corydalis yanhusuo is one of traditional Chinese medicine’s chief herbs for relieving pain. The rhizome is used. Like many Chinese herbs, it is traditionally taken as an aqueous extract (i.e., decocted as tea, although it is also given as tincture [1:3 to 1:5]) or in pill or capsule form. Substitution of other species of Corydalis for C. yanhusuo is not recommended because their actions appear to differ. Its primary active constituents are alkaloids, including berberine, corydaline, and tetrahydropalmatine. Various studies have compared Corydalis extracts to morphine and findings vary, indicating that they have from 1% to 40% the analgesic effect of morphine.16,22,54 General pain: A controlled clinical trial found that Corydalis improved pain and intensity during cold pressor testing.38 Besides its antinociceptive effects, Corydalis may be especially suited to generalized pain in cancer. On its own, Corydalis exhibits antimetastatic, antiproliferative, and antiangiogenic activity in vitro, the latter apparently via inhibition of the VEGF pathway.55 A study of the synergistic effects of Corydalis and Curcuma wenyujin found that combining the herbs in a 3:2 ratio had stronger anticancer effects than either components used singly.56

Dysmenorrhea: A study of corydaline found it effective in relieving dysmenorrhea in 73% of subjects.22 Dosage: Crude herb, decocted: 4.5 to 12 g per day, divided doses. Tincture: (1:2 to 1:5) 0.25 to 1 mL three times daily.6 Caution/contraindication: In Chinese medicine, this herb is generally contraindicated during pregnancy.16 Cannabis sativa The active constituents of Cannabis sativa (marijuana) are primarily cannabinoids, found in the greatest quantity in the flowering/ fruiting tops of the plant. Many cannabinoids have been identified, the most well-known of which is tetrahydrocannabinol (THC). As an herb, Cannabis is most commonly taken by smoking or vaporizing, eating the plant, often in other foods, or via oromucosal sprays or capsules. The herb itself is illegal under United States federal law, although some states permit its prescription. Many studies performed on Cannabis have used a synthetic form of THC (most notably dronabinol [Marinol]) or other cannabinoids such as cannabidiol (CBD), although whole herb administration and plant extracts have also been studied. Research into the mechanism of cannabinoid receptors in the body is ongoing, but suggests that they play a role in the painmediating effects of cannabinoids. Two major types of receptors, CB1 (found primarily in the nervous system, both centrally and peripherally) and CB2 (found in nonnervous tissues, including immune cells), have been identified.57 Acute postsurgical pain: A dose-escalation study showed that 10 mg of Cannabis extract (with defined THC and CBD content in a 1:0.5 ratio) administered postsurgically provided rescue analgesia after opioid administration had been discontinued.58 Neuropathic pain: Some studies of cannabinoid treatment in endof-life pain management have also been performed, often by using dronabinol. Cannabis has also been shown to improve muscle and nerve in HIV patients and the cannabinoid CT-3 was shown to have effect on neuropathic pain in end-of-life care.53 Cannabinoids were also found to be effective in managing neuropathic pain59 in conditions such as diabetic neuropathy,60 brachial plexus avulsion,61 and multiple sclerosis62 (in which cannabinoids have also been seen to subjectively improve symptoms of spasticity).63 Improved sleep: At least two studies also show increased sleep quality with Cannabis administration, which is likely to be of benefit in pain management.7 Rheumatoid arthritis: A preliminary placebo-controlled trial found that a standardized Cannabis extract (2.7 mg THC and 2.5 mg CBD per dose) significantly reduced symptoms of pain and inhibited disease progression in rheumatoid arthritis.64 Severe pain management: Opioids are regarded as the most effective therapy for severe pain, but adverse effects and tolerance may pose significant problems with their use. Besides the analgesic effects of Cannabis, which occur on a pathway independent of that of the opiates, it may also be used in concert with opioids to treat severe pain. Non-psychoactive doses of THC may act as opiate-sparing agents, just as THC acts synergistically with opioids and mediates effects of opioid tolerance. This may allow for reduced dosing of opiates to treat major pain and fewer adverse effects of tolerance.65,66 Dosage: Further study is necessary to establish dosing guidelines.

Herbal and Nutritional Supplements for Painful Conditions  195

Contraindications: Use of Cannabis, especially in adolescents and people at risk for mental illness, may be related to onset of psychological diseases such as psychosis or schizophrenia.67,68 Cautions: Although dosage has not been well-established, a study examining the effects of smoking Cannabis on capsaicin-induced pain demonstrated hyperalgesia at high Cannabis doses,69 suggesting that a therapeutic window should be established. Caution in patients with hepatitis C is warranted because Cannabis smoked daily may hasten progression of hepatic fibrosis.70 Hypericum perforatum (St. John’s Wort) The aerial parts of the plant are used as medicine. Hypericum may be given internally as a tincture, decoction, or encapsulation, or used topically as a lotion. Hypericin, hyperforin, and flavonoids are thought to be the major active constituents. This herb is most commonly associated with treatment of depression but eclectic physicians used it topically as a vulnerary and internally to treat neurogenic pain, including sciatica and rheumatic pain.71 Two murine studies demonstrated antinociceptive properties of H. perforatum. These properties are dose-dependent in a bell-shaped trend, i.e., therapeutic effect may only be derived from doses that are neither too low nor too high. Hypericum’s mechanism of nociceptive action seems to be due to hypericin’s inhibition of protein kinase C and to interaction with opioid receptors, although other receptor classes may be involved.72 Opioid receptor involvement is supported by the finding that the herb significantly enhances the effects of concurrently administered morphine without altering serum morphine levels.47 Otitis media: An herbal ear drop, of which Hypericum was the primary analgesic herb, was as effective as an ametocaine (tetracaine)/ lidocaine ear drop in relieving pain of acute otitis media.73 A double-blind, randomized study of the same product found that it was more effective used alone than with amoxicillin. This latter finding supports the use of the herbal formula as a topical treatment in acute otitis media. Pain is largely self-limiting, and current American Academy of Otolaryngology-Head and Neck Surgery guidelines recommend topical treatment as first-line therapy for this condition.74 Burning mouth syndrome: Encapsulated Hypericum reduced the number of sites of pain in stomatodynia (a condition thought to have a strong association to depressive symptoms), although the pain itself, measured by VAS scoring, was not ameliorated.75 Neuropathy: A murine study reported that even a single dose of dried Hypericum extract significantly reduced neuropathic pain in both constriction injury and chemically-induced pain.76 A human study found that Hypericum had no effect on neuropathy,77 but as the authors of the murine noted, the human neuropathy trial likely used a dose (in that study, 2700 mcg of a product called totalhypericin) of Hypericum that exceed the window of efficacy; Hypericum’s antinociceptive activity seems to follow a bell-shaped trend.76 Dosage: Tincture: (1:2 to 1:5) 2 to 4 mL three or more times per day. Decoction: 2 to 4 g dried herb taken three or more times per day. Standardized extract: 300 mg three or more times daily providing 0.3% hypericin and 5% hyperforin. Caution/contraindications: Hypericum decreased circulating warfarin levels in a study of healthy volunteers via its effects on cytochrome P450 enzymes, leading to lower PT-INR and

increased risk of clot formation in such patients. Hypericum does not affect baseline INR, only heparin clearance.78 Caution: Hypericum upregulates cytochrome P450 3A4 and possibly 2C9 and P-glycoprotein. It has been shown to reduce serum levels of drugs metabolized by P450 3A4 in the gut, although study data are limited. Drugs for which an interaction has been shown include anti-HIV protease inhibitors, cyclosporine, atorvastatin, simvastatin, finasteride, digoxin, and many others.79 In addition, the herb may reduce the efficacy of oral contraceptives; during Hypericum administration, other modes of back-up contraception should be considered. Hypericin-containing medicines may have photosensitizing effects at high doses and in very lightskinned people, although the doses recommended generally do not cause a problem.12 If there is a concern about this problem, wearing sunscreen will reduce the already low risk to nearly zero. Bryonia alba (White Bryony) The root is usually tinctured to make medicine and has traditionally been used for pleurisy, pain, and other inflammatory conditions. Bryonia dioica (red bryony) has the same effects as B. alba and may be substituted. This herb is prescribed in low doses only and is toxic in high concentrations. Gastric distress is the most common early sign of toxicity, although cardiac toxicity may result from excessive administration. Dosage: (1:10) one drop in approximately 120 mL three times daily. Caution/contraindications: Contraindicated in children, pregnancy, lactation, renal failure, and hepatic failure.6

Topical Herbs and Supplements Capsicum frutescens (Cayenne) Capsaicin is the major active constituent of the cayenne pepper, Capsicum frutescens and Capsicum annuum. It is chiefly applied topically, either in patches or in ointment form. Commercial creams or ointments are available in 0.025% and 0.075% capsaicin concentrations. Capsaicin works as a counterirritant. It stimulates small-diameter pain fibers, thereby depleting them of substance P and preventing transmission of pain signals from the peripheral to the central nervous system.22 In studies of treatment for peripheral neuropathy, for instance, patients experienced benefit after 4 to 6 weeks of use, although a high-dose topical patch resulted in immediate improvement in one study.80 Some studies concluded that capsaicin was a poor therapy but application of capsaicin was observed only for 3 or 4 weeks. Patients may experience adverse effects on initial use. Successful treatment with capsaicin has been most commonly reported in conditions affecting topical nerves, including postherpetic neuralgia,53 diabetic neuropathy, arthritis, mouth pain following chemotherapy and radiation, postmastectomy pain, and trigeminal neuralgia. However, capsicum has also been used to successfully treat cluster headaches after intranasal application.81 Dosage: Typically requires application two or three times a day or pain sensation may return. Contraindications: Capsaicin causes topical irritation on initial application, but this almost always passes with frequent use. The irritation is almost never severe. To achieve a therapeutic effect, patients must often overcome an initial period of discomfort before desensitization has occurred. Avoid contact with mucous membranes if not indicated for treatment.

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Urtica dioica (Stinging Nettle) All parts of the Urtica plant are used as medicine, although only the leaves are used to treat pain. Fresh leaves are used topically for pain as a counterirritant. Urtica leaves are covered with fine hairs with a high silicon content that break when touched and release a toxin into the skin. Like apitherapy, therapeutic effect is achieved by stinging the affected area (urtication). The toxin contains several chemicals including histamine, acetylcholine, and serotonin, and provokes urticaria and C fiber discharge.82 Joint pain: A double-blind, crossover trial of patients with chronic base-of-thumb pain due to osteoarthritis, rheumatoid arthritis, or ankylosing spondylitis found that urtication resulted in decreased disability levels and pain symptoms.83 Dosage: Topical: apply fresh leaf to affected area for approximately 30 seconds two or three times. Repeat as needed. Caution/contraindications: Theoretically, internal use may decrease efficacy of warfarin due to nettle leaf ’s substantial vitamin K content.71 Symphytum officinale (Comfrey) Herbalists have long used Symphytum root and leaf topically and internally for treatment of pain and osseous fractures. Symphytum is available in cream, ointment, and gel forms for topical use. Active constituents include rosmarinic acid, mucopolysaccharides, allantoin, and mucilage. The discovery of unsaturated pyrrolizidine alkaloids (uPA), which are potentially hepatotoxic and carcinogenic, in Symphytum has led to the recommendation that this herb be used only topically and on intact skin. uPA are absorbed only very minimally during dermal application. The herb is still used internally for short periods because studies indicate that the alkaloids cause genetic damage only in long-term use (several months or more).71,84 uPA-free extracts may be used indefinitely. Back pain: Topical Symphytum (250 g herb to 100 g cream) resulted in significantly decreased levels of pain with active motion, at rest and on palpation in patients with upper and lower back pain. The effect was strongest with higher doses, and treatment was well tolerated in all patients.85 Osteoarthritis: An ointment containing liquid extract of Symphytum root (1:2) brought about significant reduction in pain scores for knee osteoarthritis in a double-blind, placebo-controlled trial.86 Dosage: 1-2 g cream applied topically three to five times per day. Caution/contraindications: uPA-containing extracts pose a minor risk of hepatotoxicity and carcinogenicity, although these alkaloids show only minimal transdermal absorption. uPAfree extracts pose no such risk. Do not apply to large areas of broken skin. Arnica montana The Arnica flower is used topically for treatment of pain and is not generally taken internally (except in homeopathic form) because of its potential toxicity. It is available commercially in gels and ointments for topical use. Active constituents include sesquiterpene lactones, flavonoids, and volatile oils. Bruising: A rater-blinded study of 20% topical Arnica ointment found that the ointment decreased bruise healing time more than did petrolatum jelly or 1% vitamin K/0.3% retinol mixture.87 Osteoarthritis: A gel preparation of Arnica tincture was as effective in relieving hand osteoarthritis pain as ibuprofen.88

Dosage: Apply topically 3 to 5 times per day. Caution/contraindications: Not to be taken internally or applied to broken skin or near the mouth. Contraindicated in pregnancy in physiologic doses. Homeopathic topical preparations do not pose risk of toxicity in pregnancy. Dimethyl Sulfoxide (DMSO) DMSO is an organic solvent with a variety of pharmaceutical actions, including analgesic, diuretic, bacteriostatic, membranepenetrant, antiinflammatory, vasodilatory, and cholinesterase inhibitory effects.89 Data about DMSO’s analgesic effects on its own are mixed. However, when DMSO is used as a carrier for other analgesics, it increases these agents’ efficacy (in one study, lidocaine,90 in another, diclofenac)91 and reduces their morbidity. CRPS: DMSO is recommended for type I CRPS, in particular the warm type, concurrent with therapeutic exercise. Weaker evidence suggests that it may be of benefit for type II CRPS. Dosage: Applied topically five times per day.92 Caution/contraindications: May cause skin irritation. Echinacea spp. (Purple Coneflower) The aerial parts of Echinacea may be tinctured and used as a gargle. Besides its use as an antimicrobial, extracts of Echinacea can have a numbing effect and may be used to treat pharyngeal pain. An Echinacea/sage throat spray was found to be as effective and as well-tolerated as chlorhexidine/lidocaine in treatment of acute sore throats.93 Dosage: Throat spray: Two puffs every 2 hours for duration of symptoms. Tincture of fresh root (1:2 to 1:3) 3 to 5 mL in water as a gargle (then swallow) every 2 hours for duration of symptoms. Caution/contraindications: Contraindication in allergy to members of the Asteraceae (Compositae) family.

Salicylate-Containing Herbal Medicines Salix alba (White Willow) The bark of Salix alba is used for pain. Other Salix species, including S. daphnoides and S. purpurea, have a higher salicylate content, but S. alba is the most well-studied of the genus and of the salicylate-containing herbs in general. Low back pain: A Cochrane review showed moderate evidence that a 240 mg dose of salicin relieves acute exacerbations of chronic back pain and produced the same results as 12.5 mg rofecoxib.94 Effect on nonspecific low back pain is dose-dependent, with the best response seen with a 240 mg dose compared to 120 mg.94 Osteoarthritis: Salix bark extract showed benefit in relieving pain of hip and knee osteoarthritis. After 3 weeks, results were comparable to standard treatment (which was not described), and after 6 weeks, results with Salix were superior to that of the standard treatment. Mild pain complaints responded better than did those that were more severe.95 Dosage: Standardized extract providing 120-240 mg salicin per day in divided doses. Fluid extract (1:1): 2 to 4 mL three times per day or more. Tincture (1:2): 3 to 5 mL three to five times per day. Contraindications: Salicylate allergy. There is no evidence that willow causes or promotes Reye’s syndrome; indeed, the evidence that aspirin causes the disease is weak or nonexistent.96

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Populus tremuloides (Quaking Aspen) This bark of this tree and leaves contain salicylate glycosides related to those found in willow. Although they have been shown to decrease inflammation in vitro, human trials are lacking.97,98

Hypnotic Analgesic Herbs and Supplements Valeriana officianalis (Valerian) Although Valeriana is more commonly associated with treatment of insomnia, it has also traditionally been used for treatment of general pain and headache.6,99 Dosage: Tincture (1:2 or 1:3) 3 to 5 mL three times daily with 5 to 10 mL at bedtime, 1:2 to 1:3 extract. Standardized extract: (0.5% essential oil) 500 to 1000 mg three times per day and at bedtime. Cautions/contraindications: Occasionally, Valeriana may cause agitation.6 Piscidia piscipula, P. erythrina (Jamaican Dogwood) Used traditionally to treat pain, these Piscidia species are antispasmodic, hypnotic, and anodyne. The medicinal part, the root bark, is taken as a crude herb, tinctured or administered as an aqueous extract. Aqueous extract appears to be the most potent of the extractions.100 Active constituents primarily appear to be rotenoids and isoflavones, the latter category including piscidone, piscerythrone, and tetrahydroxy-methoxy-diisoprenyl-isoflavone (DPI). These herbs are commonly used in medical herbalist practice, for example for migraine, dysmenorrhea, rheumatic pain, neuralgia, sciatica, and spastic pain, but few human studies have been performed to evaluate their use. Animal studies demonstrate that the fluid extract decreases the amplitude of intestinal contractions.101 DPI, piscidone and piscerythrone had spasmolytic effects against oxytocin-induced contractions in rat uteri.102 Symptoms of toxicity include sweating, numbness, tremors, and excessive salivation. Dosage: Crude root bark (dried): 2 to 4 g three times daily. Tincture: (1:3 to 1:5) 1 to 3 mL three or more times per day. Caution/contraindications: Caution: Dosing simultaneously with other sedative therapies, as Piscidia may amplify these effects. Contraindication: pregnancy, bradycardia, and cardiac insufficiency. Eschscholtzia californica (California Poppy) The aerial parts of the plant have been used as a hypnotic anodyne traditionally. Its hypnotic effects have been confirmed in the research literature, but few comprehensive clinical studies have been performed on Eschscholtzia to examine its role in pain management. It is taken internally, most commonly as a tincture or decoction.6 Although a member of the Papaveraceae family, it is traditionally regarded as one of the safest and most gentle of the anodynes and may be given to children.103 Dosage: Tincture (1:2): 3 to 5 mL three or more times per day. Caution/contraindications: German Commission E monographs indicate a caution for use in pregnancy because cryptopine, a minor constituent, causes uterine stimulation in animal studies. No such activity, however, has been observed after administration of Eschscholtzia.21

Nutritional Cofactors Methylsulfonylmethane (MSM) MSM is produced by the adrenal glands and may be obtained in the diet from some fruits and vegetables. Arthritides: MSM shows weak pain-relieving effect on its own but is more frequently given in conjunction with glucosamine with or without chondroitin. Animal studies showed that it decreased joint degeneration. Thus far, human studies showed modest effects on pain and swelling, but no effect on stiffness.104 Dosage: 1000 to 3000 mg three times per day. Caution/contraindications: None currently noted. Riboflavin This B vitamin serves a variety of metabolic roles. With regard to pain control, its mechanism is similar to that of coQ10 in that it facilitates mitochondrial energy metabolism. Migraine: High-dose riboflavin (400 mg per day) reduced frequency of attacks and number of days of migraine duration.105,106 Dosage: 400 mg per day. Caution/contraindications: None. Lipoic Acid/Alpha Lipoic Acid/Thioctic Acid Lipoic acid is a disulfide produced in the body. It is a small, easily absorbed molecule and is a potent antioxidant that increases the activity of catalase and superoxide dismutase in peripheral nerves, is neurogenerative and normalizes endoneural blood flow. Because it is both lipophilic and hydrophilic, it addresses both fatand water-soluble free radical species. It is administered orally and intravenously. Coadministration of a B-complex supplement is recommended because lipoic acid may deplete these vitamins.107 Migraine prophylaxis: Thought to have an effect similar to riboflavin and coQ10, thioctic acid showed within-group improvement in headache days, frequency, and severity of migraines in one study.108 Research is ongoing, and anecdotal reports are favorable.53 Diabetic neuropathy: A critical review of several clinical trials of varying sizes found that intravenous lipoic acid significantly improved major symptoms of diabetic polyneuropathy, including that of the cranial nerves;53 lower limb motor and sensory nerve conduction; and deficits in nervous function and cardiac autonomic neuropathy. Furthermore, it reversed some of the vascular changes of diabetes, including elevated NF-κB, albuminuria, and elevated thrombomodulin. The analysis did not reveal any major concerns about safety.107 A long-term study (NATHAN I) is being conducted to further assess the role of lipoic acid in treatment of diabetic polyneuropathy. Dosage: 600 to 1800 mg orally per day in divided doses; 600 mg daily intravenously. Caution/contraindications: May worsen paresthesias when treatment is first begun. May decrease blood glucose levels.53 S-adenosyl methionine (SAM-e) SAM-e is the stable salt form of S-adenosyl methionine, a methyl donor produced from methionine and adenosine triphosphate in the liver. It is commonly used to treat depression, a condition in which CSF SAM-e levels tend to be low, compared to nondepressed individuals.109 SAM-e increases turnover of serotonin and may increase levels of dopamine and norepinephrine.

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Osteoarthritis: SAM-e controlled osteoarthritic pain as effectively as celecoxib after 2 months of use in a study comparing the two, although celecoxib controlled pain much better in the first month.104

Pediatric migraine: An intention-to-treat analysis of magnesium oxide administration found a significant reduction in migraine days compared to placebo.119

Fibromyalgia: A double-blind, placebo-controlled Danish study found that 800 mg of SAM-e administered orally improved fatigue, disease activity, morning stiffness, mood, and pain experienced during the study’s final week.110

Dysmenorrhea: Magnesium likely inhibits prostaglandins and was found to be superior to placebo in the treatment of dysmenorrhea.120

Dosage: 800 to 1600 mg per day in divided dose.

Dosage of elemental magnesium: Children: 9 mg/kg/day; Adults: 250 to 600 mg per day in divided doses, to bowel tolerance.

Caution/contraindications: Rare episodes of mania and hypomania have been reported in depressed patients taking SAM-e. Drugherb interactions may occur with concurrent administration of serotonergic drugs, levodopa, or monoamine oxidase inhibitors.

Caution/contraindications: Magnesium citrate supplements can have an osmotic laxative effect at high doses. This effect may be seen to a lesser degree in other forms.

Glucosamine Sulfate and Chondroitin Sulfate Although they are not anodynes in the same sense as other remedies listed here, glucosamine sulfate and chondroitin sulfate are useful in the treatment of osteoarthritis pain because of their effect on joint structure. Glucosamine is a substrate for the glycosaminoglycans that comprise hyaluronic acid, a chief component of joint tissue. Chondroitin plays a number of roles in connective tissue synthesis. It is itself a glycosaminoglycan and, when hydrated, it creates osmotic pressure that increases the compressive resistance of synovial cartilage. It also stimulates the production of collagen and proteoglycan and inhibits enzymatic destruction of the synovium.22,111

Melatonin Research on melatonin has examined the hormone’s influence on nonendocrine tissues and has elucidated the mechanism by which it might influence pain. It is present throughout the central nervous system, and has been shown to treat acute, inflammatory, and neuropathic pain symptoms.121

Osteoarthritis: Numerous studies have been performed to evaluate the efficacy of glucosamine and chondroitin administration for osteoarthritis treatment with mixed results, although this may be due to combining different forms of the agents, or to some studies’ use of less effective forms of glucosamine and/or chondroitin or products with poor standardization.53 Industry bias may also account for some of the discrepancy between studies, although it should also be noted that many of the studies not funded by industry sources examined glucosamine hydrochloride.112 According to a meta-analysis, glucosamine sulfate used alone relieved pain due to osteoarthritis and prevented disease progression.113 Glucosamine hydrochloride, although cheaper, is not effective for osteoarthritis.114 Conclusions derived from studies of one form cannot be extrapolated to apply to the other form, even though data for glucosamine sulfate are mixed.115 Chondroitin treatment reduced pain, swelling, and effusion, and maintained or improved joint space and serum osteocalcin levels. Glucosamine sulfate and chondroitin sulfate taken together decreased pain and joint effusion in moderate-to-severe arthritis pain, but results were inconsistent between studies.111,116 Dosage: 1500 mg glucosamine sulfate per day. 400 to 1200 mg chondroitin sulfate per day. Caution/contraindication: Contraindication for glucosamine: shellfish or iodine allergy. Glucosamine may increase PT-INR when given with warfarin.117 Chondroitin may also increase the effects of anticoagulant therapies. Because of its structural similarities to heparin, some sources recommend that it be contraindicated in pregnancy.118 Magnesium Used clinically for a wide range of conditions, magnesium is given in a variety of forms, including magnesium citrate, glycinate, and oxide. Food sources include green leafy vegetables, whole grains, nuts, and seeds.

Hormonal Analgesics

Migraines/headaches: Melatonin levels are frequently low in migraineurs and cluster headache patients.122 Many of the symptoms of migraine prodrome seem to originate in the hypothalamus, which exerts regulatory input over the pineal gland and its melatonin production. Melatonin is also present in significant amounts in the trigeminal ganglion, which may also be involved in migraine initiation. It is unknown if melatonin plays a direct role in headache pathogenesis, or if decreased melatonin simply is another sign of hypothalamic dysfunction, but melatonin treatment has been shown to ameliorate headache symptoms in some individuals,123 especially those with clear circadian dysregulation (i.e., delayed sleep phase syndrome).22 Postoperative analgesia: A randomized, placebo-controlled study found that patients undergoing elective prostatectomy who were given 6 mg melatonin the night before and 1 hour before surgery had less pain, used less intraoperative fentanyl, required less tramadol, and had better postoperative sleep than the placebo group. The treatment group, however, had greater extubation time and took longer to recover from anesthesia.124 Dosage: 1 to 20 mg, generally taken only at bedtime or just before a painful procedure. Caution/contraindications: May cause daytime grogginess and delayed recovery from anesthesia. Vitamin D Although vitamin D is a nonessential vitamin, recent research has demonstrated epidemic deficiency of this vitamin in the general population, especially in the elderly, institutionalized populations, those who live in northern latitudes, with limited sun exposure or who have dark skin. It is available in pill, capsule, powder, and liquid forms. Vitamin D deficiency has been linked with a variety of painful disease states, including bone loss and attendant fractures,125 pelvic floor disorders,126 systemic lupus erythematosus,127 tuberculosis, certain cancers, and inflammatory bowel diseases.128 A 2008 review article, however, found that studies demonstrating a link between hypovitaminosis D and chronic pain were largely of poor quality and that too few randomized controlled trials had been performed.129 Although vitamin D2 (ergocalciferol) and D3 (cholecalciferol) are both available commercially, the D3 form of the vitamin is more potent and has longer-lasting effects.130

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Vitamin D intoxication is reported rarely, and published cases all involve persons who consumed at least 40,000 IU per day longterm. Evidence suggests that the currently accepted No Adverse Effect Limit of 2000 IU per day is probably too low “by at least five fold.” No adverse effects are seen in individuals who are not hypersensitive when serum levels of 25(OH)D are less than 140 nmol/L (56 ng/mL), which is attained in healthy people by consuming 10,000 IU per day long term.131 Another study whose subjects’ serum concentrations reached 400 nmol/L reported no observable hypercalcemia, hypercalciuria or adverse effects.132 Although dosages of 10,000 IU per day may be taken long-term without major problems, very large single doses of vitamin D are not recommended. A study in which a massive single dose of vitamin D (500,000 IU) was given to women older than age 70 with normal baseline serum levels demonstrated that such high doses increased the risk of fracture and falling.133 Osteomalacia: Supplemental vitamin D is crucial to treatment of osteomalacia, as hypovitaminosis D is a key component of the disease’s pathogenesis. Pain may worsen before improvement is seen following treatment.134 Diabetic neuropathy: Type 2 diabetics are commonly deficient in vitamin D. Repletion of vitamin D levels in these patients resulted in significant reduction of neuropathic pain. Pain scores were negatively correlated with serum 25(OH)D levels, although no correlation between pain and serum iPTH levels was observed.135 Low back pain: A study of 360 Saudi Arabian men and women with low back pain of no obvious etiology found that 83% had deficient levels of vitamin D.136 Another reported a similar finding among Egyptian women.137 However, treatment was not performed as part of either study. Rheumatoid arthritis: A vitamin D receptor has been identified on human immune cells. In its capacity as a hormone, vitamin D seems to downregulate autoimmunity caused by excessive Th-1 activity. Serum 25(OH)D levels are inversely correlated with disease activity in rheumatoid arthritis. People with autoimmune diseases may have a higher vitamin D requirement to maintain optimum serum levels.138,139 Myalgia in statin-treated patients: 92% of statin-treated patients with concurrent myalgia/myositis and hypovitaminosis D saw resolution of myalgia/myositis after 12 weeks of 50,000 IU vitamin D per week (the form of the vitamin given was not identified).140 Migraine: Case studies report successful treatment of menstrual and postmenopausal migraine with vitamin D and calcium, although no large-scale studies have so far been performed.141,142 Multiple sclerosis: The Nurses’ Health Study demonstrated that women whose serum vitamin D levels were in the highest quintile were 40% less likely to develop multiple sclerosis.138 Dosage: Vitamin D3, or cholecalciferol, is the preferred form. Recommended daily allowances are 200 to 600 IU per day, depending on age, with a maximum safe level of 2000 IU per day, but evidence suggests that doses necessary to treat deficiency and even to maintain normal levels are much higher (5,000 to 20,000 IU per day). Due to interactions between these vitamins in vivo, it is recommended to give high-dose vitamin D with small amounts of vitamins A and K.143 Therapeutic dose: 1000 to 10,000 IU per day long term. Weekly doses of 50,000 IU are also given, usually for shorter durations (e.g., 4 to 6 weeks).

Caution/contraindications: Contraindications: Hypercalcemia, hyperphosphatemia, vitamin D toxicity, and sarcoidosis. Caution in calcium oxalate nephrolithiasis. Coenzyme Q10 (CoQ10) Coenzyme Q10 acts as a mitochondrial electron-transport chain cofactor in the reactions that produce ATP. It scavenges free radicals and is a component of the Krebs cycle enzyme succinate dehydrogenase-coQ10. Its alternate name, ubiquinone, reflects its omnipresence throughout the body. Despite the fact that coQ10 is synthesized innately, it is commonly deficient in the general popu­ lation.22 Its production decreases with age and it is depleted by many pharmaceuticals, including beta blockers, antipsychotics, some statins, metformin, sulfonylureas, and some tricyclic antidepressants.118 Animal studies demonstrate that its antinociceptive effects may be a consequence of its downregulation of nitric oxide.144 Two forms are available commercially—ubiquinone and ubiquinol (ubiquinone’s reduced form). Ubiquinol is more commonly given clinically. Migraines: CoQ10 deficiency may be a predisposing factor in the incidence of migraine headaches.145 Prophylactic coQ10 supplementation in adult migraineurs146 and repletion of coQ10 in pediatric migraineurs with low serum levels decreased migraine frequency.147 Chronic Fatigue Syndrome: Although the role of oxidative stress and mitochondrial dysfunction in chronic fatigue syndrome is controversial, coQ10 levels were found to be low in such patients. Supplementation may improve symptoms of chronic fatigue syndrome.148 Dosage: Pediatric: 1 to 3 mg/kg/day. Adults: 150 mg/day with food. Caution/contraindications: Antagonizes warfarin and other anticoagulants, may increase effect of hypotensives.118

Miscellaneous Agents Ginkgo biloba (Ginkgo) Ginkgo is most commonly prescribed for vascular disorders, including those pertaining to perfusion of the central nervous system. The leaves are used in Western herbalism, and the seed kernel is used in traditional Chinese herbal medicine. Active constituents include ginkgolides A, B, C, and J (all diterpene lactones), bilobalide (a sesquiterpene lactone), and flavonol glycosides. Ginkgo is available as tincture, capsules, tablets, decoction, and standardized extract— usually in solid form. The standardized extract is the most wellresearched preparation and contains 24% to 32% flavonoids and 6% to 12% terpenoids. The standardized extract form is the most recommended by some sources because proportions of active constituents may vary widely between different samples of crude herb. Migraine: A preliminary trial found that an extract containing ginkgolide B reduced frequency and duration of migraine attacks in adults.149 Another preliminary trial found that Ginkgolide B given prophylactically with coQ10, vitamin B2 and magnesium reduced frequency and need for pain medication in a small group of pediatric migraineurs.150 Raynaud’s phenomenon/disease: A standardized extract of Ginkgo was effective in reducing number of attacks in patients with Raynaud’s phenomenon compared to placebo.151 Anecdotal evidence also suggests effectiveness in Raynaud’s disease of the nipple during lactation.

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Intermittent claudication: A 2000 meta-analysis found that Ginkgo extract was slightly more effective than placebo in increasing walking distance, although not as effective as vasodilators.152 A more recent Cochrane review, however, found that Ginkgo offered no benefit in treatment of this condition.153 Dosage: Standardized extract: 120 to 240 mg per day, in divided doses. Caution/contraindications: Ginkgo should be discontinued at least 36 hours prior to surgery. It may interact additively with other anticoagulants.71 Drug-herb interactions are possible with a number of other pharmaceuticals, including anticonvulsants, antidepressants, cyclosporine, and thiazide diuretics. Centella asiatica (Gotu Kola) Centella has been used in traditional herbal medicines across Asia. The whole plant is used, and dosage forms include encapsulation of the crude herb, decoction, and tinctures. Active constituents include triterpenoid saponins and notable amounts of asiaticoside, madecassoside and madecassic acid. A murine study demonstrated that the crude herb possesses antiinflammatory and antinociceptive properties. Its effects were likely mediated by the central and peripheral nervous systems and its mechanism of action may involve opioid receptors.154 Venous insufficiency: Centella has been used traditionally for its circulatory effects. A triterpene fraction of Centella given to patients with venous hypertension decreased symptoms of edema, pain, fatigue, and restless limb more effectively than placebo. Capillary filtration rate was also decreased, as was ankle circumference, in patients receiving the Centella extract.155 Dosage: 180 mg per day of total triterpenic fraction. Tincture or glycerite of fresh plant (1:2 to 1:3) 3 to 5 mL three or more times per day. Topical cream 1-2 g two or more times per day. Caution/contraindications: Caution in patients with cholestasis, celiac disease, fat malabsorption disorders, and deficiency of fatsoluble vitamins due to Centella’s high saponin content.21 Viburnum opulus (Cramp Bark), Viburnum prunifolium (Black Haw) The bark of both species is used medicinally and may be decocted, tinctured, or encapsulated as crude herb. Viburnum opulus contains hydroquinones, coumarins, and tannins, whereas Viburnum prunifolium’s primary constituents include coumarins, biflavones, and phenolic acids. Dysmenorrhea: Both Viburnum species treat dysmenorrhea, although classically, V. opulus is used for pain radiating into the thighs and V. prunifolium is specific for severe low back pain with a feeling of bearing down in the pelvis. Animal studies demonstrate that both herbs have relaxant effects on the uterus, and this effect has also been described in humans in studies of V. prunifolium.156 Dosage: V. opulus: Tincture: 5 to 10 mL (1:5) three times per day. Encapsulated or decocted crude herb: 2 to 4 g three times per day. V. prunifolium: Tincture: (1:3 to 1:5) 5 to 10 mL (1:5) three times per day. Encapsulated or decocted: 2.5 to 5 g three times per day. Cautions/contraindications: Caution: V. prunifolium is also used to treat hypertension; use caution in hypotensive patients. This herb also contains oxalates but is generally given in doses far too low to warrant caution in patients with calcium oxalate nephrolithiasis.

Scutellaria laterifolia (Skullcap) Scutellaria baicalensis (Huang qin) This herb has been part of traditional Chinese materia medica for millennia and is used to treat pain and inflammatory conditions. Its active constituents include baicalin, a flavonoid, the herb’s most studied component. Osteoarthritis: A short-term, randomized, double-blind study found that a supplement (flavocoxid, given 500 mg twice per day) combining baicalin and catechin (a flavan derived from Acacia catechu) was as effective as naproxen in treating osteoarthritic knee pain. The mechanism of action is likely inhibition of COX-2, LOX-5 and NF-κB.157 Dosage: Dried herb: 1 to 2 g three times per day. Liquid extract (1:2): 0.6 to 1.5 mL three times per day. Tincture (1:5): 1 to 2 mL three times per day.6 Caution/contraindications: Not to be used for extended periods during pregnancy.21 Rosa canina The fruit is used medicinally and is taken internally as a decoction, alcohol extract, powder, or encapsulated. Rosa fruits generally contain high concentrations of vitamin C, although their antioxidant properties result from other components as well. Osteoarthritis: A clinical trial of a powder made from Rosa canina was found to reduce osteoarthritic pain compared to placebo.158 A meta-analysis found Rosa powder to be twice as likely as placebo to reduce pain.159 Dosage: 4 to 5 g powder twice daily. Caution/contraindications: None currently known. Solidago chilensis (Brazilian Arnica) The leaves and flowers of Solidago have long been used as medicine by indigenous Brazilians. Active constituents include flavonoids, carotenes, and diterpenoids. Mouse studies demonstrate that the rhizome also possesses potent antiinflammatory activity.160 Low back pain: In a small, placebo-controlled study, Solidago improved lumbar flexibility and reduced pain when applied topically in gel form. The majority of the subjects experienced absence of pain with treatment.161 Dosage: 10 g gel applied topically twice daily. Caution/contraindications: Allergy to members of the Asteraceae family. REFERENCES 1. Bücker B, Groenewold M, Schoefer Y, Schäfer T. The use of complementary alternative medicine (CAM) in 1 001 German adults: Results of a population-based telephone survey. Gesundheitswesen. 2008;70(8-9):e29-e36. 2. Ebbell B. The Papyrus Ebers: The Greatest Egyptian Medical Document. Copenhagen: Levin & Munskgaard; 1937. 3. Court WE. A history of herbal medicine. Pharm Hist (Lond). 1985;15(2):6-8. 4. Yang S, Dennehy CE, Tsourounis C. Characterizing adverse events reported to the California Poison Control System on herbal remedies and dietary supplements: A pilot study. J Herb Pharmacother. 2002;2(3):1-11. 5. Woolf AD, Watson WA, Smolinske S, Litovitz T. The severity of toxic reactions to ephedra: Comparisons to other botanical products and national trends from 1993-2002. Clin Toxicol (Phila). 2005;43(5):347-355.

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126. Badalian SS, Rosenbaum PF. Vitamin D and pelvic floor disorders in women: Results from the National Health and Nutrition Examination Survey. Obstet Gynecol. 2010;115(4):795-803. 127. Ruiz-Irastorza G, Egurbide MV, Olivares N, et al. Vitamin D deficiency in systemic lupus erythematosus: prevalence, predictors and clinical consequences. Rheumatology. 2008;47:920-923. 128. Zittermann A. Vitamin D in preventive medicine: are we ignoring the evidence? Br J Nutrition. 2003;89:552-572. 129. Straube S, Andrew Moore R, Derry S, et al. Vitamin D and chronic pain. 2009;141:10-13. 130. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89: 5387-5391. 131. Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations and safety. Am J Clin Nutr. 1999;69:842-856. 132. Kimball SM, Ursell MR, O’Connor P, Vieth R. Safety of vitamin D3 in adults with multiple sclerosis. Am J Clin Nutr. 2007;86:645-651. 133. Sanders KM, Stuart AL, Williamson EJ, et al. Annual high dose oral vitamin D and falls and fractures in older women: A randomized controlled trial. JAMA. 2010;303:1815-1822. 134. Goldman L, Ausiello D, eds. Goldman Cecil Medicine. 23rd ed. Philadelphia: Saunders; 2008. 135. Lee P, Chen R. Vitamin D as an analgesic for patients with type 2 diabetes and neuropathic pain. Arch Intern Med. 2008;168:771-772. 136. Al Faraj S. Al Mutairi K: Vitamin D deficiency and chronic low back pain in Saudi Arabia. Spine. 2003;28:177-179. 137. Lofti A, Abdel-Nasser AM, Hamdy A, et al. Hypovitaminosis D in female patients with chronic low back pain. Clin Rheumatol. 2007;26:1895-1901. 138. Cutolo M, Otsa K, Uprus M, et al. Vitamin D in rheumatoid arthritis. Autoimmun Rev. 2007;7:59-64. 139. Mouyis M, Ostor AJ, Crisp AJ, et al. Hypovitaminosis D among rheumatology outpatients in clinical practice. Rheumatology. 2008;47(9):1348-1351. 140. Ahmed W, Khan N, Glueck CJ, et al. Low serum 25 (OH) vitamin D levels (<32 ng/mL) associated with reversible myositis-myalgia in statin-treated patients. Trans Res. 2009;153:11-16. 141. Thys-Jacobs S. Vitamin D and calcium in menstrual migraine. Headache. 1994;34:544-546. 142. Thys-Jacobs S. Alleviation of migraines with therapeutic vitamin D and calcium. Headache. 1994;34:590-592. 143. Pizzorno JE. The path ahead: What have we learned about vitamin D dosing? Integrative Med. 2010;9:8-12. 144. Jung HJ, Park EH, Lim CJ. Evaluation of anti-angiogenic, anti-­ inflammatory and antinociceptive activity of coenzyme Q(10) in experimental animals. J Pharm Pharmacol. 2009;61(10):1391-1395. 145. Hershey AD, Powers SW, Vockell AL, et al. Coenzyme Q10 deficiency and response to supplementation in pediatric and adolescent migraine. Headache. 2007;47(1):73-80. 146. Rozen TD, Oshinsky ML, Gebeline CA, et al. Open label trial of coenzyme Q10 as a migraine preventative. Cephalagia. 2002;22:137-141. 147. Lewis DW. Pediatric migraine. Neurol Clin. 2009;27(2):481-502. 148. Cordero MD, De Miguel M, Moreno Fernàndez AM, et al. Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients: Implications in the pathogenesis of the disease. Arthritis Res Ther. 2010;12(1):R17[Epub ahead of print]. 149. D’Andrea G, Bussone G, Allais G, et al. Efficacy of ginkgolide B in the prophylaxis of migraine with aura. Neurol Sci. 2009;(Suppl 1):S121-S124. 150. Usai S, Grazzi L, Andrasik F, Bussone G. An innovative approach for migraine prevention in young age: A preliminary study. Neurol Sci. 2010;31(Suppl 1):181-183. 151. Muir AH, Robb R, McLaren M, et al. The use of Ginkgo biloba in Raynaud’s disease: A double-blind placebo-controlled trial. Vasc Med. 2002;7:265-267. 152. Moher D, Pham B, Ausejo M, et al. Pharmacological management of intermittent claudication: A meta-analysis of randomised trials. Drugs. 2000;59(5):1057-1070.

20

204  Complementary and Alternative Medical Procedures 153. Nicolaï SP, Kruidenier LM, Bendermacher BL, et al. Ginkgo biloba for intermittent claudication. Cochrane Database Syst Rev. 2009;15: CD006888. 154. Somchit MN, Sulaiman MR, Zuraini A, et al. Antinociceptive and anti-inflammatory effects of Centella asiatica. Indian J Pharmacol. 2004;36:377-380. 155. De Sanctis MT, Belcaro G, Incandela L, et al. Treatment of edema and increased capillary filtration in venous hypertension with total triterpenic fraction of Centella asiatica: A clinical, prospective, placebocontrolled, randomized, dose-ranging trial. Angiology. 2001;52(Suppl 2): S55-S59. 156. Hudson T. Women’s encyclopedia of natural medicine. 3rd ed. London: Churchill Livingstone; 2005. 157. Levy RM, Saikovsky R, Shmidt E, et al. Flavocoxid is as effective as naproxen for managing the signs and symptoms of osteoarthritis in the knee in humans: A short-term randomized, double-blind pilot study. Nutr Res. 2009;29:298-304.

158. Rein E, Kharazmi A, Winther K: A herbal remedy, Herben Vital (stand. powder of a subspecies of Rosa canina fruits), reduces pain and improves general wellbeing in patients with osteoarthritis–a doubleblind, placebo-controlled, randomised trial. Phytomedicine. 2004;11: 383-391. 159. Christensen R, Bartels EM, Altman RD, et al. Does the hip powder of Rosa canina (rosehip) reduce pain in osteoarthritis patients?—a meta-analysis of randomized controlled trials. Osteoarthr Cartilage. 2008;16:965-972. 160. Liz R, Vigil SV, Goulart S, et al. The anti-inflammatory modulatory role of Solidago chilensis Meyen in the murine model of the air pouch. J Pharm Pharmacol. 2008;60:515-521. 161. da Silva AG, de Sousa CP, Koehler J, et al. Evaluation of an extract of Brazilian arnica (Solidago chilensis Meyen, Asteraceae) in treating lumbago. Phytother Res. 2010;24:283-287.

21

Body Work and Movement Therapies Alex Moroz, MD, FACP, Marissa H. Cohler, MD, and Robert A. Schulman, MD Since the 1960s, alternative forms of pain management have become progressively more popular and widely available. Complementary and alternative medicine, also known as CAM, emphasizes a holistic approach to the treatment of pain, in contrast to its traditional medical counterparts that takes a more unimodal approach. These alternative methods include yoga, massage, tai chi chuan, Alexander technique, body awareness therapy, and Pilates, and all offer noninvasive approaches to pain. Usually, these therapies are criticized on the grounds that they are rarely analyzed by methodologically sound, controlled clinical trials and their effects cannot be administered by doctors with confidence. However, there are numerous studies on these alternative forms of pain management and a majority of trials and reports have demonstrated positive correlations between the techniques and pain relief.

Yoga Yoga is an Indian art created by the sage Patanjali, approximately 2000 years ago to “see things as they really are and achieve freedom from suffering.”1 The details of the meditative program of yoga were chronicled in the Yoga sutra, written by Patanjali. A partly philosophical work, the sutra explores the nature and reason for human suffering and offers yoga as a potential remedy. Patanjali explains yoga as a vehicle for connecting with the external world, as well as for understanding the internal world. Despite the spiritual nature of yoga, the art is nonsectarian; traditionally, yoga was passed on directly from teacher to student.2 Classically, yoga is described as eight connecting limbs. The first limb is Yama, moral and ethical behavior. This limb consists of Ahimsa (nonviolence), Sayta (truth), Asteya (honesty), Brahmacharya (temperance and chastity), and Aparigraha (noncovetousness). The second limb is Niyama, personal behavior. Niyama can be broken down into Saucha (purity), Santosa (contentment), Tapas (austerity), Svadhyaya (introspection), and Isvara Pranidhana (yielding to a higher being). Asana, or posture, is the third limb. This limb consists of specifically designed physical postures that effectively stimulate the body (Fig. 21-1). Such postures are often named after the nature, mythological being, or body part they resemble, such as “the Lotus,” “Hanumanasana,” and “headstand,” respectively.3 The postures allow for the fourth limb, Pranayama, or breath control. The limb consists of a refined control of drawing air into the body and expelling it

to expand what is known as Prana (life-force). Pratyahara, sensory inhibition, is the fifth limb. It involves managing the senses to allow the body to use them to look inward. The next limb is Darana, or concentration. This limb involves steady concentration on a specific item without interruption. The seventh limb of yoga is Dhyana, meditation. Meditation is the ability to maintain one’s attention without being distracted. The final limb is Samadhi or ecstasy. This limb involves transcending oneself in all aspects and coming to understand ultimate truth.4 Yoga’s call for the specific control of body has allowed its’ practitioners to perform seemingly supernormal acts: “The voluntarily stopping and restarting of the heart, the holding of breath for extended periods, the ability to remain motionless for months or even years, and the prolongation of life itself are well-known examples.”5 Each Asana has its own respective benefits (Fig. 21-2). Four connected examples of Asanas include Sarvangasana, Halasana, Bhujangasana, and Matsyendrasana. Sarvangasana is the shoulder stand posture; it involves resting the body on the shoulders and neck. Generally, blood circulation is improved in this posture, allowing a large supply of blood to the upper extremities. In addition, the posture eliminates the stiffness caused by long periods of standing. Halasana proceeds after Sarvangasana; the feet are positioned behind the head.6 This position completely stretches the spine and helps reduce constipation by increasing the movement of the intestines through compression. Bhujangasana is also known as the “cobra” posture and counteracts the forward bending of the previous two postures. Essentially, in this posture, the stomach lies to the ground with legs straight, while the neck is stretched backwards. As a result, the muscles of the neck are strengthened and the chest is stretched. Matsyendrasana continues the posture by allowing for the rotary flexion of the spine. In this Asana, the participant sits on the floor and brings the right heel against the perineum. The right hand then grasps the right knee, thereby allowing the body to twist. The lumbar muscles are stretched as a result of this position.7 A recent article in the Journal of Alternative and Complemen­ tary Medicine8 demonstrated the benefits of yoga on pain. Thirtythree veterans at the Veterans Administration Hospital in San Diego with chronic low back pain received weekly Anusara Yoga classes. After 10 weeks, the participants reported significant improvements in pain severity, with a mean rating of 70.94 out of 100 at baseline and 61.36 at follow-up (P < .001). There was also improvement on 205

206  Complementary and Alternative Medical Procedures

Figure 21-1  Modified child yoga position enhancing release of pelvic girdle and axial spine tension.

other parameters such as energy and depression (Table 21-1). Of note, these results reflect the thirty-three veterans who fully participated in the program, as 15 participants dropped out or were unavailable for follow-up after initial questionnaire. At the Swami Vivekananda Yoga Research Foundation in India a randomized controlled trial (RCT) comparing the effect of a short-term intensive residential yoga program with physical exercise (control) on pain and spinal flexibility was conducted in subjects with chronic low-back pain.9 The intervention consisted of a 1-week intensive residential yoga program composed of Asanas designed for back pain, Pranayamas, meditation, and didactic and interactive sessions on philosophical concepts of yoga. The control group practiced physical exercises under a trained physiatrist and also had didactic and interactive sessions on lifestyle change. Hourto-hour matching for the types of practices for the two groups was ensured (see Table 21-2). After 7 days, there was a significant reduction in pain scores (as measured by the Oswestry Disability Index) in the yoga group compared to the control group (P = .01; effect size 1.264). In a pilot study of adults (mean age 59 years) with osteoarthritis of the knee where all participants received the intervention of yoga, Kolasinski and colleagues found statistically significant reductions in pain (a decrease of 47% over 8 weeks).10 The clinic-based intervention consisted of 90-minute sessions delivered weekly over an 8-week period. Of the 11 subjects enrolled, 7 (64%) completed at least five of the eight classes and underwent both pre- and postin­ tervention assessments. In an RCT conducted at West Virginia University School of Medicine, the investigators randomized 60 adults with chronic low back pain (mean age 48.3 years, low back pain for 11.2 ± 1.54 years) to weekly yoga classes (1.5 hours/week) or an education control group over 16 weeks.11 Pain was assessed using the Short FormMcGill Pain Questionnaire (SF-MPQ).12 The SF-MPQ measures present pain intensity with a standard horizontal 10 cm visual analog scale (VAS)13 and the Present Pain Index (PPI). The VAS is a bipolar line scale with the descriptive anchors of no pain on the left side of the line and worst possible pain on the right side of the line. The PPI is a rating scale that requires each patient to endorse their pain with one check from 0 representing no pain to 5 representing excruciating pain. Forty-two (70%) subjects completed the study. At 3-month follow-up, the control group VAS rating was 2.0, whereas

Figure 21-2  Yoga position facilitating stretching.

for the yoga group it was 0.6 (P = .039). The PPI rating was also significantly less in the yoga group than the control (0.5 versus 1.1, respectively, P = .013). Additionally, significantly more people in the yoga group stopped or decreased use of pain medication than the control group. A study at the Group Health Cooperative,14 a nonprofit, integrated healthcare system in Washington and Idaho, enrolled 101 primary care patients (mean age, 44 years) with chronic back pain and randomized them to receive either 12 weeks of yoga, 12 weeks of a structured exercise class, or an education only group (participants were given a book on self-care for back pain). The participants were followed-up at 6, 12, and 26 weeks with a telephone interview and were asked, among other things, to rate from 0 to 10 how bothersome their pain had been during the previous week. All groups had decreased bothersome symptom scores at 26 weeks (see Fig. 21-3). No significant differences in bothersome symptoms were found between any two groups at 12 weeks; at 26 weeks, the yoga group was superior to the book group with respect to this measure (mean difference,− 2.2 [CI, −3.2 to −1.2]; P < .001), however there were no significant differences between the yoga and exercise groups. At the University of Sao Paolo in Brazil 40 women with fibromyalgia were randomized to receive either relaxing yoga (RY) or relaxing yoga plus touch (RYT)—touch being the manipulative techniques of Tui Na.15 Both groups received weekly sessions for 8 weeks and showed improved pain scores. Touch addition yielded greater improvement during the treatment. Over time, however, RY patients reported less pain than RYT. These results suggest that a passive therapy may possibly decrease control over fibromyalgia symptoms. Morone and colleagues16 conducted a structured review of eight mind-body interventions for older adults with chronic

Body Work and Movement Therapies  207

21

Table 21-1  Mean Scores on Health Questionnaires N

Mean at Baseline

Mean at 10-Week Follow-up

Mean Change

SD of the ­Difference

P

Effect Size*

Pain

33

70.94

61.36

–9.57

12.90

<0.001

0.74

Energy

33

2.02

2.66

0.64

0.89

<0.001

0.72

Depression

33

14.53

10.67

–3.87

5.29

<0.001

0.73

SF12-PCS

29

36.10

37.68

1.58

9.48

0.376

0.17

SF12-MCS

29

40.77

45.53

4.77

11.13

0.029

0.43

*Effect sizes are Cohen’s “d” (small = 0.20, medium = 0.50, large = 0.80). SD, Standard deviation; SF-12, Medical Outcomes Study Short-Form 12; PCS, Physical Composite Score; MCS, Mental Composite Score. From Groessl EJ, Weingart KR, Aschbacher K, et al: Yoga for veterans with chronic low-back pain. J Altern Complement Med 2008;14(9):1123-1129.

Table 21-2  Timetable for the Yoga and Control Groups: Daily Schedule Step Number

Time

Yoga Group

Control Group

1

5:00-5:30 am

Om meditation—30 min

Walking—30 min

2

5:30-06:30 am

Yoga-based special technique—60 min

Exercise-based special technique—60 min

3

6:30-7:30 am

Bathe

Bathe

4

07:30-08:15 am

Chanting of yogic hymns—45 min

Video show (on nature)—45 min

5

08:15-08:45 am

Breakfast

Breakfast

6

08:45-10:00 am

Rest

Rest

7

10:00-11:00 am

Lecture (on yogic lifestyle)—60 min

Lecture (on healthy lifestyle)—60 min

8

11:00-12:00 noon

Pranayama (yogic breathing)—60 min

Non-yogic breathing practice—60 min

9

12:00-01:00 pm

Yoga-based special technique—60 min

Exercise based special technique—60 min

10

01:00-02:00 pm

Lunch (vegetarian diet)

Lunch (vegetarian diet)

11

02:00-02:30 pm

Deep relaxation technique—30 min

Rest at room—30 min

12

02:30-04:00 pm

Assessments and counseling

Assessments and counseling

13

04:00-05:00 pm

Cyclic meditation—60 min

Listening to music—60 min

14

06:15-06:45 pm

Divine hymns session (Bhajan)—30 min

Video show (on nature)—30 min

15

06:45-07:45 pm

Meditation with yogic chants (mind sound resonance technique)—45 min

Walking—45 min

16

07:45-08:30 pm

Dinner (vegetarian diet)

Dinner (vegetarian diet)

17

08:30-10:00 pm

Self-study

Self-study

From Tekur P, Singphow C, Nagendra HR, Raghuram N. Effect of short-term intensive yoga program on pain, functional disability and spinal flexibility in chronic low back pain: A randomized control study. J Altern Complement Med 2008;14(6):637-644.

nonmalignant pain. Of the articles that met criteria of studying older adults (>50 years) with chronic pain, they found that yoga was significantly associated with pain reduction for low back pain, osteoarthritis, and carpal tunnel syndrome. See Table 21-3 for summaries of the included studies. Researchers at the University of Rajasthan17 examined yoga’s impact on migraine in an RCT. Seventy-two patients (mean age, 34, females > males) who had been diagnosed with migraine without aura were assigned to attend yoga or self-care groups for 12 weeks. After this time, the yoga group was statistically significantly less on all parameters measured (P < .001): headache frequency (4.56 versus 10.18 days in the last month), average pain score (4.64 versus 7.81 out of 10) and duration of attacks (4.78 versus 6.42 hours). Additionally, on the SF-MPQ pain questionnaire, the yoga group was significantly less in overall intensity of pain (1.69 versus 3.97).

Garfinkel and colleagues18 conducted a randomized controlled multicenter trial of Hatha Yoga for patients with carpal tunnel syndrome, emphasizing upper body postures and relaxation. The control group was assigned to wear wrist splints for 8 weeks. Participation in the yoga program was for 60 to 90 minutes, two times per week for 8 weeks. Average pain intensity in the subjects in the yoga group, as measured by the VAS, decreased from 5.0 to 2.9 after 8 weeks (P = .02), whereas pain did not significantly decrease in the control group. The authors of a follow-up article theorized that yoga may decrease wrist and hand pain by improving posture and reducing compression on the median nerve.19 Garfinkel also examined the effect of yoga on osteoarthritis pain.20 He conducted an RCT on patients with osteoarthritis who received either eight weeks of yoga (one 60-minute session

208  Complementary and Alternative Medical Procedures

Symptom bothersomeness scale score

per week focusing on stretching and strengthening of the upper body) or no therapy. The yoga-treated group improved significantly more than the control group in pain intensity during activity and tenderness. In addition to musculoskeletal pain, yoga has been found to exhibit some relief in people with cancer pain. Researchers at Duke University21 conducted a pilot study of 21 women with metastatic breast cancer and who received the Yoga Awareness Program for 8 weeks. The Yoga Awareness Program was specifically designed for metastatic breast cancer patients and included gentle yoga postures, breathing exercises, meditation, didactic presentations, and group interchange. Lagged analyses of length of home yoga practice 10 9 8 7 6 5 4 3 2 1 0

Book group Exercise group Yoga group

showed that on the day after a day during which women practiced more, they experienced significantly lower levels of pain. Yoga is an effective treatment for pain as supported by a large body of literature; its benefits have been recognized by major medical societies. According to a report issued by the American College of Physicians and the American Pain Society,22 yoga is a valid consideration for chronic or subacute low back pain in patients who have not improved with self-care options. This recommendation is largely based on the Group Health Cooperative study mentioned previously. The report grades the level of evidence as “Fair” with a moderate net benefit for Viniyoga, but “Poor” with unknown benefit for Hatha Yoga. It is unclear the mechanism by which yoga improves pain, but is likely due to a combination of stretching and physical movement with relaxation and mental focus. It is important to take note that several of these studies are confounded by noncompliance and drop-out. Yoga may relieve pain but only if those people with pain are able to and comply with practicing it.

Pilates 0

6

12

26

Week Figure 21-3  Mean symptom bothersome symptom scale scores at baseline, 6, 12, and 26 weeks by treatment group. (Adapted from: Sherman KJ, Cherkin DC, Erro J, et al: Comparing yoga, exercise, and a self-care book for chronic low back pain: a randomized, controlled trial. Ann Intern Med 2005;143:849-856.)

Pilates is a system of psychophysical exercise that was created by Joseph Pilates. It emphasizes good posture, proper breathing, body awareness, and graceful movement to better condition the body to prevent it from being prone to injury.23 Pilates was once associated with being the training method of the elite and famous. Since the 1980s, however, the training method has entered into the mainstream.

Table 21-3  Results of Several Articles Examining Effect of Yoga on Pain Reduction Design/­ Methods

≥65 Years

Kolasinski (2005)10

Pre-post

No

Sherman et al. (2005)15

RCT

No

Garfinkel et al. (1994) 20

RCT

No

Garfinkel et al. (1998)18

RCT

Study

Condition/Age/N Knee OA mean age 58 (50-68) ll N = 11

Outcome ­Measures

Pain Effect Sizes/ Quality Grade

Notes

Yoga 8 sessions

ll

Pain and ­physical function (WOMAC)*

Unable to ­compute effect size Quality: very low

36% attrition

ll

Chronic low   back pain ll mean age 44 ll N = 101

Yoga versus exercise versus self-care book ll 12 sessions

RDS* Bothersome symptoms* Medication use*

Unable to ­compute effect size Quality: high

0% attrition in yoga,   6% attrition in exercise (attrition defined as attending no classes)

OA of hands age 52-79 ll N = 25

Yoga + relaxation +   education versus wait-list ll 8 sessions

Pain (joint tenderness and hand pain ­during activity)*

Effect size Pain with ­Dolorimeter: ll 1.57 right hand, ll 1.16 left hand Quality: low

4% attrition ll Controls were crossed over into yoga

Carpal tunnel ­syndrome ll age 24-77, median 52 ll N = 51

Yoga versus usual   care + wrist splint ll 8 sessions

Pain VAS* Grip strength*

Effect size Pain VAS: ll 0.41 Quality: ­moderate

15% attrition in yoga 20% attrition in control

ll

No

Intervention/ Control/Length of Treatment

*P < .05 OA, Osteoarthritis; RCT, Randomized controlled trial; VAS, Visual analog scale. From Morone NE, Greco CM: Mind-body interventions for chronic pain in older adults: A structured review. Pain Med 2007;8:359-375.

Body Work and Movement Therapies  209

The history of Pilates began in the early 1900s while Joseph Pilates was interned in England with other German nationals. Originally working as a self-defense instructor for Scotland Yard, Pilates expanded and developed his ideas during his internment. In one particular case, he attached springs to hospital beds for immobile patients, allowing them to exercise. After the war, Pilates’ techniques become popular in the German dancing community. However, Pilates eventually decided to immigrate to the United States in 1926. By 1960, Pilates had married and worked as an instructor for ballerinas from the New York City Ballet. The popularity of his training expanded across the country. After Pilates’ death in 1967, his students, including Romana Kryzanowska, Ron Fletcher, Kathy Grant, and Lolita San Miguel, opened their own Pilates’ styled exercise studios around the country and in Puerto Rico. Notably, Ron Fletcher’s studio catered to Hollywood celebrities, greatly increasing the popularity of Pilates.24 The execution of Pilates varies depending on the equipment available as well as the aim of the user. Generally, mats and reformers, a system of springs and ropes for resistance, are most common. Variations of the exercise range from athletes who want a specific form of improvement, including running faster or throwing farther, to lay people looking to develop strength and coordination.25 In Maher’s 2004 review,26 he concluded that there is insufficient scientific evidence to justify the effectiveness of Pilates (see Table 21-1). However, randomized clinical studies of the effect of Pilates on pain have become more common over the past few years, three of which were analyzed by La Touche and colleagues27 and deemed to be of satisfactory methodology (Table 21-4). The evaluation of the methodological quality of the studies was carried out using two instruments, the PEDro28 and Jadad Scales.29 The PEDro Scale includes 11 items to evaluate four fundamental methodological aspects of a study such as the random process, the blinding technique, group comparison, and the data-analysis process. All three controlled trials included in La Touche’s analysis indicated positive effects of Pilates for alleviating chronic lower back pain.

The Donzelli study30 (see Table 21-4), an RCT, showed significant reduction in back pain after daily therapy of Pilates or back school for 10 days. Pain was assessed using the Visual Analog Scale and decreased from an average score of 6 at pretreatment to 4 at 6-month follow-up. Although Pilates was not compared directly to back school treatment, the Pilates group showed better compliance and subjective response to treatment. The Rydeard study (see Table 21-4),31 albeit small, had convincing results. After 4 weeks of Pilates practice, the posttest adjusted mean in lower back pain intensity in the specific-exercise-training group was 18.3 out of 101 (95% CI, 11.8 to 24.8), compared to 33.9 out of 101 (95% CI, 26.9 to 41.0) in the control group who received the usual care, defined as consultation with a physician and other specialists and healthcare professionals, as necessary (P  =  .002). After 12 months, however, there was no longer a significant difference in lower back pain between the two groups. Beyond the aforementioned articles, there have been few other articles examining the effectiveness of Pilates in pain relief. A pilot study by Keays and colleagues32 evaluated four women with breast cancer status post-axillary dissection and radiation therapy. Each participant received 1-hour Pilates exercise sessions three times per week for 8 weeks. Pain was assessed using the Brief Pain Inventory-Short Form (BPI),33 a 15-item, self-administered tool developed for use in patients with cancer. Results were inconclusive. Except for participant 1, high levels of pain at the study outset were not reported. Average pain level decreased by 2 to 11 points from baseline to intervention for participants 1, 3, and 4 but increased by 1 point for participant 2. There are data to suggest a positive effect of Pilates; however, it is unclear for what duration and in what contexts it is truly beneficial. Larger, RCTs are needed.

Massage Massage is the stimulation of and applied pressure on soft tissue for therapeutic purposes, and is one of the oldest forms of medical treatment in the world, with origins in various societies. Chinese writings dating back to 2700 bc and 2598 bc mention massage in

Table 21-4  Results of Several Randomized Clinical Studies Examining the Effect of Pilates on Pain Study ll

Gladwell et al. (2006)

Method ll ll

RCT Blinding assessors

Subjects ll ll

ll

ll

Donzelli et al. (2006)30

ll ll

CCT Blinding assessors

ll ll

N = 49 Age: EG average: 36; CG average: 45 All the participants, ­average: 40 N = 53 Average age: 50

Intervention ll ll

ll

ll ll ll

ll

Rydeard et al. (2006)31

ll ll

RCT Blinding assessors

ll ll

ll

N = 39 Age: EG average: 37; CG, average: 34 Sex: F 25, M 14

ll

ll

ll

ll

EG: Pilates on mat CG: Without specific intervention and with continuous health care Duration: 1 session a wk for 6 wk CG: Back school method EG: Pilates on mat Duration: 10 consecutive 1 h sessions EG: Pilates on (reformer) machines and on mat CG: Without specific intervention and with continuous health care Duration: 1 hr a week and 15 min of exercise at home 6 day/week. Complete program = 4 wk

Outcome ll

ll

ll

Significant statistical effects in improving general health, sports functions, flexibility, proprioception and reducing pain Both groups showed reduced back pain and improved function; however, there was no comparison between both groups Significant statistical effects in reducing pain and improving functions

CCT,; CG, Control group; EG, Exercise group; F, Female; M, Male; RCT, Randomized controlled trial. From La Touche R, Escalante K, Linares MT: Treating non-specific chronic low back pain through the Pilates Method. J Bodyw Mov Ther 2008;12:364-370.

21

210  Complementary and Alternative Medical Procedures

religious documents and a medical work, respectively. The depictions of massages were found on the wall of an Egyptian physician’s tomb in Saqqara circa 2330 bc. Massage was also mentioned and approved in both the Indian medical work, Ayurveda, written around 1800 bc and by Hippocrates in 400 bc in the book On Articulations. Since its origins, the popularity of massage as a form of medical treatment has fluctuated, particularly in Western civilizations. In Western civilizations, the acceptance and use of massage declined from the fifth century to the Renaissance. This was largely due to the influence of the Church; it condemned massage for bringing pleasure to the body. However, in 1819, massage became more acceptable in Western medicine when Piorry analyzed its ­physiologic effects. Modern massage came into effect when the practice became more systematic. In 1863, the French publication of Estradere’s Du Massage, “systematically classified each massage technique according to the bodily system affected.” This influenced the rise of scientific massage techniques.34 Such techniques include the Swedish massage techniques developed by Per Henrik Ling in the early nineteenth century. In the United States, modern scientific massage therapy was introduced in the mid 1800s. In the United States, massage techniques were used by physicians until the early 20th century. When the pharmaceutical revolution occurred in the 1940s, massage therapy became less acceptable and was categorized as an alternative form of health care. In the 1960s, physical therapy began to use massage for the treatment of musculoskeletal impairments and other physical impairments. During the same era, the growth in the movements toward emphasizing human psychology and spirituality greatly increased massage therapy’s popularity. Following the 1960s, massage therapy eventually became incorporated into the “normal,” healthy lifestyle. Nursing and physical therapy have come to reincorporate massage techniques including simple backrubs, reflexology, therapeutic touch, and aromatherapy massage. Presently, surveys in the United States have indicated the growing popularity of massage; it is one of the most commonly used therapies for both the general population as well as individuals with disabilities, and it is one of the top physician referrals for alternative therapies.35 Several common stroke techniques can be found among the myriad of massage techniques. These include, effleurage, friction, pressure, petrissage, vibration, and percussion. Effleurage involves rhythmic and gentle skin contact. Generally, the palm is used for larger body surfaces, whereas the fingers are used for smaller body surfaces. In the friction stroke technique, pressure is applied to one area with the thumbs or fingers in moderately. The pressure stroke is, similar to the friction stroke, except that pressure strokes are made with the hands. Petrissage, also known as kneading, involves lifting and holding skin and the underlying muscle. The tissues are pushed against the bone. Tissues are supported by one hand while kneading is done with the other hand. Kneading is generally limited to areas of the body with large muscles mass. Vibration strokes involve the use of continuous motion. For percussion strokes, the wrist is used for tapping areas of the body.36 Massage therapy to treat pain is extremely common in the United States, however, exact numbers are unclear. Sherman and others surveyed randomly selected acupuncturists, chiropractors, and massage therapists in two states.37 Back pain was the most common reason for visits to each of these providers, with chronic back pain representing about 12% of visits to massage therapists.

Wells and coworkers38 studied use of complementary and alternative therapies in 189 women with non–small-cell lung cancer. Massage was used by 6.9% of participants, most commonly for pain (54.8%). Women who were younger, experienced more symptoms, and lived on the West Coast or in the South (versus the Northeast) were more likely to use complementary and alternative therapies. In a nationally representative survey that sampled 2055 adults, Wolsko and colleagues39 discovered that 54% of those reporting back or neck pain in the last 12 months used complementary and alternative therapies, including 14% who used MT. According to Brett and colleagues, 15% of midlife U.S. women have used massage and chiropractic medicine, most commonly for pain.40 Palinkas and Kabongo41 surveyed 542 patients attending sixteen family practice clinics belonging to a community-based research network in San Diego, California, and found that 17.2% used MT. The results of a survey and interviews of older adults showed that the most prevalent motivation for using complementary and alternative therapies was pain relief (54.8%), and that MT was used by 35.7%.42 Prevalence of MT use in a large military family practice clinic was found to be 36%, most commonly used for back or other musculoskeletal pain.43 In a telephone interview survey of Chicago adults 45 years of age or more, Feinglass and others44 discovered that more than half of the respondents used complementary and alternative therapies, most commonly MT and relaxation techniques. Similarly, more than half of traumatically injured spinal cord patients with shoulder pain received MT or physical therapy.45 In terms of the benefits of massage, Ernst evaluated systematic reviews of massage therapy (MT) and chiropractic effects on reduction of any type of pain.46 Two reviews were found, and there was not unequivocal evidence for effectiveness of MT in controlling musculoskeletal or other pain. A meta-analysis of 37 studies that used random assignment concluded that single applications of MT did not reduce immediate assessment of pain, whereas multiple applications reduced delayed assessment of pain.47 Back and colleagues described a pilot program to evaluate the efficacy of employer-funded on-site massage therapy on job satisfaction, workplace stress, pain, and discomfort.48 Twenty-minute massage therapy sessions were provided weekly for 4 weeks. Evaluation demonstrated possible improvements in job satisfaction, with initial benefits in pain severity (as measured by the Brief Pain Inventory49), and the greatest benefit for individuals with preexisting symptoms. Pain severity decreased by about 2% when initially measured after the 4-week massage period. However, at followup of 6 weeks and 12 weeks, pain severity actually incrementally increased. This was thought to be due to the MT making participants more aware of their bodies and pain, thereby causing them to report higher pain scores. Use of MT in neck, back, and other musculoskeletal pain has been studied extensively. A review by Trinh and others50 concluded that there is limited evidence that MT is less effective than acupuncture in chronic mechanical neck pain. Ezzo and colleagues51 analyzed 19 trials of MT in neck pain, with 12 of 19 receiving lowquality scores. Descriptions of the massage intervention, massage professional’s credentials, or experience were frequently missing. Six trials examined massage as a stand-alone treatment. The results were inconclusive. Results were also inconclusive in 14 trials that used massage as part of a multimodal intervention because none were designed such that the relative contribution of massage could be determined.

Body Work and Movement Therapies  211

21

Table 21-5  Designs of Randomized Controlled Trials Evaluating Massage for Back Pain Study, (Year) Reference

Type and Duration of Pain

Massage

Mixed (1 wk-8 mo)

Treatments

Sample Size, n

Types of Masking

6 Treatments in 1 mo Comprehensive massage (soft tissue manipulation plus remedial exercise) Soft tissue manipulation Remedial exercise Sham laser therapy

1. 26 27

Not stated

24 27

Preyde (2000)33

Mixed (>6 wk: most patients had pain for >1 yr)

≤10 treatments over 10 wk Massage Acupuncture Self-care educational materials

78 94 90

Assessor

Hernandez-Reif (2001)77

Chronic (≥6 mo)

2 treatments per week for 5 wk Massage Progressive muscle relaxation

12 12

Not stated

From Cherkin DC, Sherman KJ, Deyo RA, Shekelle PG: A review of the evidence for the effectiveness, safety, and cost of acupuncture, massage therapy, and spinal manipulation for back pain. Ann Int Med 2003;138(11):898-906.

Table 21-6  Results of Randomized Controlled Trials Evaluating Massage for Back Pain Primary Outcomes

Follow-up

Function, pain

At end of 1-mo treatment   period and again 1 mo later

Follow-up >85% Yes

Results At 1 mo follow-up, both comprehensive massage and soft tissue manipulation were superior to sham laser for pain and function and superior to exercise for pain (all P <.05). Comprehensive massage and soft tissue manipulation did not significantly differ.

Dysfunction, ­bothersome­ ­symptoms

4, 5, and 52 wk after ­randomization

Yes

At 10 wk, massage was superior to acupuncture (dysfunction,   P = .01) and self-care education (symptoms, P = .01 dysfunction, P <.001). After 1 yr, massage was superior to acupuncture (dysfunction, P = .05; symptoms, P = .002) but did not differ significantly from self-care ­education.

Pain, depression, anxiety, sleep, flexion, ­serotonin levels, ­dopamine levels

Immediately after   treatment period

Not stated

Massage group reported less pain (P <.05) and depression (P = .05), improved sleep (P = .03), and flexion (P <.003), and higher serotonin and dopamine levels (both P = .04).

From Cherkin DC, Sherman KJ, Deyo RA, Shekelle PG: A review of the evidence for the effectiveness, safety, and cost of acupuncture, massage therapy, and spinal manipulation for back pain. Ann Int Med 2003;138(11):898-906.

Cherkin and co-authors52 reviewed Medline, Embase, and the Cochrane Controlled Trials Register, and included three RCTs that evaluated massage and reported that this therapy is effective for subacute and chronic back pain and superior to certain other therapies (Tables 21-5 and 21-6). For example, Hernandez-Reif compared massage therapy to muscle relaxation. Twelve patients with chronic low back pain were randomly assigned to each of these treatments. After ten 30-minute sessions over 5 weeks, massage was found to be superior to progressive muscle relaxation for pain, depression, flexion, and sleep. Similarly, Furlan and colleagues53 conducted a systematic review of Medline, Embase, Cochrane Controlled Trials Register, HealthSTAR, CINAHL, and dissertation abstracts describing use of MT for lower back pain. Nine publications reporting on eight randomized trials were included. Three had low and five had high methodological quality scores. Massage was compared with an inert treatment (sham laser) in one study that demonstrated massage was superior, especially if given in combination with exercises

and education. In the other seven studies, massage was compared with different active treatments. They showed that massage was inferior to manipulation and transcutaneous electrical nerve stimulation; massage was equal to corsets and exercises; and massage was superior to relaxation therapy, acupuncture, and self-care education. The beneficial effects of massage in patients with chronic LBP lasted at least 1 year after the end of the treatment. One study comparing two different techniques of massage concluded in favor of acupuncture massage over classic (Swedish) massage. A review of several modalities including MT in the management of painful musculoskeletal disorders54 concluded that, although evidence from basic science research suggests many of the therapies could have potentially therapeutic effects, there is limited high-quality evidence from randomized clinical trials to support the therapeutic effectiveness of these therapies. Best and colleagues reviewed evidence for using massage for muscle and soft tissue pain and weakness after intense exercise.55 Analysis of 27 studies that met inclusion criteria led authors

212  Complementary and Alternative Medical Procedures

to conclude that, although case series provide little support for the use of massage to aid muscle recovery or performance after intense exercise, randomized controlled trials provide moderate data supporting its use to facilitate recovery from repetitive muscular contractions. It also appears that the experience of the massage therapist may be directly related to effectiveness of the MT in relieving muscle soreness after a 10 km race.56 Dryden and associates57 reviewed evidence for using massage in orthopedic problems and concluded that massage therapy may be effective for orthopedic patients with low back problems and potentially beneficial for patients with other orthopedic problems. Massage therapy appears to be safe, to have high patient satisfaction, and to reduce pain and dysfunction. In a randomized, double blind, placebo controlled trial of 140 subjects with knee osteoarthritis, physiotherapy including MT appeared no more effective in reducing pain at 12 and 24 weeks than regular contact with a therapist.58 Several investigators have studied use of massage in cancer pain. Ferrell-Torry and Glick59 administered thirty minutes of therapeutic massage on two consecutive evenings to nine hospitalized males diagnosed with cancer and experiencing cancer pain. Massage therapy significantly reduced the subjects‘ level of pain perception and anxiety. In addition to these subjective measures, all physiologic measures (heart rate, respiratory rate, and blood pressure) tended to decrease from baseline, providing further indication of relaxation. Building on the work of these authors, Grealish and colleagues60 administered 10-minute foot massage (5 minutes per foot) to 87 subjects hospitalized with cancer and found a significant immediate effect on the perceptions of pain, nausea, and relaxation when measured with a visual analog scale. In a larger study, the impact of a Swedish massage intervention on 251 oncology in-patients‘ (mean age, 54.96) perceived level of distress.61 The analysis found a statistically significant reduction in patient-reported distress for both pain and physical discomfort by 43% and 47%, respectively, regardless of gender, age, ethnicity, or cancer type (P = .000). Jane and colleagues62 reviewed 15 studies published in English between 1986 and 2006 for study design, methods, and massage efficacy in adult patients with cancer. Methodological issues identified included less rigorous inclusion criteria, failure to consider potential confounding variables, less than rigorous research designs, inconsistent massage doses and protocols, measurement errors related to sensitivity of instruments and timing of measurements, and inadequate statistical power. Use of massage by caregivers during cancer treatment in children has also been reported.63 There is a distinct body of literature describing the use of MT in puerperal and neonatal periods. Several investigators agree that massage is effective in reducing low back and labor pain, particularly during early stages of labor.64-66 Additionally, it appears that perineal massage during labor may prevent third-degree but not first- and second-degree perineal tears.67 Sensorial saturation including massage was studied by Bellieni and co-authors, and found to be an effective analgesic technique during minor painful procedures on newborns.68 Experience of the provider did not seem to make a difference.69 Use of massage for post-operative pain control has been addressed by several authors. Forchuk and colleagues70 evaluated the usefulness of arm massage from a significant other following lymph node dissection surgery in a randomized clinical trial that included 59 women. Participants reported a reduction in pain in

the immediate postoperative period and better shoulder function. Anderson and Cutshall71 reviewed benefits of massage in the reduction of pain, anxiety, and tension in cardiac surgical patients and described a clinical case example of a patient who has experienced cardiac surgery and received massage therapy[M5]. He complained of persistent pain in the sternum, shoulder, and back following surgery despite increased doses of pain medication. After a 20-minute massage session, the patient reported his pain decreased from 7 to 2 on the VAS. The authors argue that MT can serve as a postsurgical pain blocker by modulating pain transmission in nerves. It may activate impulses in larger diameter nonpain fibers that block transmission in smaller diameter pain-fibers that travel to the spinal cord. This is based on Melzack and Wall’s gate-control theory of pain.72 In a study attempting to test the effectiveness of physiotherapy-based rehabilitation starting 1 week after lumbar disc surgery, Erdogmus and co-authors73 compared “comprehensive” physiotherapy, “sham” neck massage, and no therapy. Low back pain at 12 weeks was equally improved in the comprehensive and the sham massage groups, compared to controls. In a randomized trial of MT in 605 veterans with acute postoperative pain after major surgery, Mitchinson and others74 found that compared with the control group, patients in the massage group experienced short-term decreases in pain intensity (P = .001), pain unpleasantness (P < .001), and anxiety (P = .007). In addition, patients in the massage group experienced a faster rate of decrease in pain intensity (P = .02) and unpleasantness (P = .01) during the first 4 postoperative days compared with the control group. Another area that deserves discussion is use of massage in patients with pain related to burn injuries. Field and colleagues75 randomly assigned 28 adult patients with burns before débridement to either a massage therapy group or a standard treatment control group. Massage therapy group demonstrated decreased pain on the McGill Pain Questionnaire, Present Pain Intensity scale, and Visual Analog Scale. In their review, Gallagher and colleagues76 described massage as one of the nonpharmacologic modalities routinely used in treating patients with burns. Hernandez-Reif and others77 studied 24 young children (mean age, 2.5 years) hospitalized for severe burns who received standard dressing care or massage therapy in addition to standard dressing care prior to dressing changes. The massage therapy was conducted on body parts that were not burned. During the dressing change, the children who received massage therapy showed minimal distress behaviors and no increase in movement other than torso movement. In contrast, the children who did not receive massage therapy responded to the dressing change procedure with increased facial grimacing, torso movement, crying, leg movement, and reaching out. Nurses also reported greater ease in completing the dressing change procedure for the children in the massage therapy group. Schneider and colleagues78 described massage as a common alleviating factor in their review of neuropathic-like pain after burn injury. Overall, it seems that massage therapy has a beneficial effect in a variety of types and contexts of pain. It should be considered by physicians as an alternative or complementary therapy to conventional pain management techniques. Of course, the skills and training of massage therapists vary widely and it is imperative that patients and their doctors take great care when choosing a practitioner.

Body Work and Movement Therapies  213

21

Figure 21-4  “Single Whip” Tai Chi posture.

Tai Chi Tai Chi Chuan is a martial art rooted in the philosophy of Daoism that emphasizes fluid, continuous movement (Fig. 21-4). Literally translated as the “supreme ultimate fist,”79 Tai Chi Chuan strives for balance and harmony in the practitioners’ movements vis-à-vis Chi or Qi, the metaphysical life force that Daoism believes to run through all living beings. Through the correct positioning of the body, the gracefully proper transitions between positions, as well as mental concentration, Tai Chi Chuan aims for harmony within the practitioner and between the practitioner and way of nature (Fig. 21-5). Because the emphasis of Tai Chi Chuan is precise and fluid motion, it can be practiced by a wide range of age groups.80 The way of nature is a fundamental aspect of both Daoism and Tai Chi Chuan. The quintessential book of Daoism, the Dao De Jing, states that the Dao has no set form but can be understood through the cyclical movement of nature as well as through the opposite, yet complementary forces in nature.81 The Dao has been described as being, “like empty space, but emptiness has been undervalued, since the hollow in the center of a bowl, the space in a wheel between rim and hub, or the empty space of a window or door in a room are the very things which give these objects their point and usefulness.” In essence, the passiveness of the Dao helps the flow of Chi in the body.82 The recorded history of Tai Chi Chuan begins in the 17th century, a transition period between the Ming and Qing dynasties. The art of Tai Chi Chuan was a secret and closely protected heirloom of the Chen family. This pattern was broken around the 19th century when Yang Luchan, the first notably nonmember of the Chen family, learned the art from Chen Changxing. Eventually Yang made his own contributions to the art, leading to the creation of the Yang style. Proliferation of Tai Chi Chuan continued and as a result, multiple variations of Tai Chi Chuan exist today, with the Chen, Yang, Sun, Wu, and alternative Wu, as the more popular of the variations.83 Tai Chi Chuan practice is based on the following 10 principles created by Grand Master Yang Chen-Fu in the late 1920s: 1. K  eep the head and neck straight (as if suspended from above) 2. U  pper and lower back is kept in a straight line with the pelvis tucked in

Figure 21-5  “Separate Left” Tai Chi posture.

3. W  aist is relaxed and rotates easily, including the muscles of the hips and groin 4. S  houlders and elbows are relaxed and sinking down 5. U  pper and lower parts of the body always move as one coordinated unit 6. A  lways differentiate between a full (solid) and an empty leg when moving (i.e., be aware to which leg a weight shifting is occurring) 7. M  ove using only the intention of the mind and no external muscle force 8. M  ake each movement flow into the next in a smooth, continuous manner 9. A  ssure a sense of harmony between the internal and external body feeling 10. E  xperience a tranquil, meditative state84 From these principles, the actual practice of Tai Chi Chuan begins with warm-up exercises such as foot massages and gentle patting of the face, neck and arms; this is done to stimulate the movement of chi. The final part of the warm-up involves the “waving arms” exercise; the exercise involves shifting the body weight among the legs and other parts of the body as well as free swinging of the arms in a backwards motion. After the warm-up, the exercises begin. Common to all the variations of Tai Chi Chuan is the review. At the beginning of each session, previous motions are reviewed to ensure they have been practiced adequately and that the motions are correct. Typically, a session lasts between 60 to 90 minutes in length.85

214  Complementary and Alternative Medical Procedures

Table 21-7  Synopsis of Level I and Level II Evidence Investigating Therapeutic Benefits of Taiji By Research Design, Subject, Intervention, Salient Findings, and Score for Methodologic Rigor (MR) Study Authors (Year Published)

Design Subjects

Intervention

Results

Irwin et al.42 (2003)

Level I RCT, 36 older adults

20 Tai chi movements,   15 wk, 3 times/wk 45-min classes ­compared with ­wait-listed controls

Significant increases in: SF-36 scores for role-physical and physical ­functioning and varicella zoster virus-specific ­cell-­mediated immunity (↑ 50%) in Taiji group

MR Score 42.5

Hartman et al.36 (2000)

Level I RCT, 33 adults with lower limb osteoarthritis

Nine-form Yang style,   12 wk, twice-weekly ­supervised exercise compared with controls instructed to maintain normal activity

Taiji group experienced significant increases in self-efficacy for arthritis symptoms, total arthritic self-efficacy, level of tension, and satisfaction with general health status

44.5

Bhatti et al.32 (1998)

Level I RCT, 51 adults with a diagnosis of chronic back pain

11 Taiji movements, 6 wk, once-weekly supervised exercises compared with controls

Significant reductions in average, lowest, and worst pain experienced in the last week and mood improvement

36.5

Li et al.46 (2001)

Level I RCT, 94 seniors

24 simplified form Yang style, 6 mo, twice weekly compared with controls instructed to maintain normal activity

Taiji group reported significant ­improvements in physical functioning

Adler et al.58 (2000)

Level I RCT, 16 adults diagnosed with chronic arthritis pain

Traditional Wu-style form Tai Chi, 10 wk, once-weekly supervised exercise compared with controls instructed to maintain normal activity

Taiji group pain intensity scores ­significantly decreased as compared with controls; no changes in ­­quality-­  of-life score were found

33.5

Young et al.59 (1999)

Level I RCT, 62 ­sedentary older adults

Mini lecture and instruction in 13 movements from Yang style, 12 wk, ­twice-weekly supervised exercise ­augmented with home exercise compared with controls engaged in program of aerobic activities

Both groups had reductions in systolic and diastolic blood pressure (systolic blood pressure adjusted mean changes of -7.0 for Taiji group and −8.4 for exercise group; diastolic blood pressure adjusted mean changes of -2.4 for Taiji group and −3.2 for exercise group); body fat did not change in either group

42.5

Wolf et al.60 (1997)

Level I RCT, 72 inactive older adults (a subgroup of the FICSIT trials)

Ten movements from 108-form Yang style, 15 wk, twice-weekly supervised exercise compared with a balance training group and a control group

Balance training group had significant improvement in platform balance ­measures; Taiji group members were less afraid of falling

40

Channer et al.27 (1996)

Level I RCT, 126 patients 3 wk ­postdischarge after acute myocardial­ ­infarction

Wu Chian-Ch’uan Jaiji, 11 sessions over 8 wk as ­compares with aerobic exercising group and ­nonexercising support group

Taiji group showed trends in ­decreasing diastolic blood pressure; Taiji, and aerobic exercising groups both showed trends in systolic blood pressure ­lowering; Taiji group had high exercise program persistence

40

Wolf et al.61 (1996)

Level I RCT, 200 seniors ≥70 yr, FICSIT

Ten movements from 108-form Yang style, 15 wk, twice-weekly supervised exercise compared with a balance training group and a control group

Taiji was found to reduce risk of falls by 47.5% and lower blood pressure; no s­ignificant changes were seen across intervention groups in ­remaining biomedical, functional status, and ­psychosocial variables

41

Sun et al.62 (1996)

Level I RCT, 20 among older adults ≥60 yr

Mini lecture and Taiji movements, 12 wk, once-weekly supervised exercise compare with controls instructed to maintain normal activities

Lower resting systolic and diastolic blood pressures, reduction in perceived stress, and increase in shoulder and knee flexibility

40

Brown et al.63 (1995)

Level I RCT, 180 healthy older   sedentary adults

Taiji-type activity with visual imagery, 16 wk, 2 times/wk of supervised exercise compared with moderate-intensity ­walking, low-intensity walking, low intensity walking plus relaxation response or control

Psychological benefits; women in visual imagery Taiji-type activity group ­experienced reductions in mood ­disturbances; women in moderateintensity walking group noted greater ­satisfaction with physical attributes; men in the moderate-intensity walking group reported increased positive affect

39

43

Body Work and Movement Therapies  215

21

Table 21-7  Synopsis of Level I and Level II Evidence Investigating Therapeutic Benefits of Taiji By Research Design, Subject, Intervention, Salient Findings, and Score for Methodologic Rigor (MR)—cont’d Study Authors (Year Published) Jin64 (1992)

Design Subjects

Intervention

Results

Level I RCT, 96 Taiji ­practitioners

Long form, Yang style, or Wu style Taiji, one Taiji episode compared with brisk walking, or meditation and neutral reading

After all treatments, salivary cortisol levels dropped significantly; stress reduction measure by heart rate, blood pressure, and urinary catecholamine changes for Taiji group were similar to those for brisk walking group

MR Score 42

RCT, Randomized controlled trial. Controlled research evidence confirming therapeutic benefits of Tai Chi practice with regard to pain management. From Klein PJ, Adams WD: Comprehensive therapeutic benefits of Taiji: A critical review. AmJ Phys Med Rehab 2004;83(9):735-745.

Comprehensive benefits of Tai Chi were reviewed by Klein and Adams.86 Of more than 200 published reports examined, 17 controlled clinical trials were judged to meet a high standard of methodological rigor. Controlled research evidence was found to confirm therapeutic benefits of Tai Chi practice with regard to pain management (Table 21-7). Use of Tai Chi among other mind-body interventions in neurology patients was reviewed by Wahbeh and others.87 Authors discussed applications of mind-body therapy to general pain, back and neck pain, carpal tunnel syndrome, headaches, and fibromyalgia, and concluded that the evidence for the efficacy of mind-body therapies is quite strong in some conditions, such as migraine headache. Research-based use of Tai Chi for reducing pain and stress as a potential nursing intervention was summarized by Chen and ­Snyder.88 Authors critically evaluated existing literature and suggested that additional studies about the effects of Tai Chi from a nursing perspective are needed to make clear when it is beneficial as a nursing intervention. Conversely, Siu and and coworkers89 used Tai Chi as a control intervention in a study evaluating a 6-week Chronic Disease Self-Management Program (CDSMP) in 148 subjects with chronic illness. CDSMP subjects used more cognitive methods to manage pain and had a tendency to adopt the cognitive methods of diverting attention, reinterpreting pain, ignoring sensations, and making positive self-statements, when compared with subjects assigned to the Tai Chi (control) group. A number of investigators studied the effectiveness of Tai Chi in patients with osteoarthritis pain. Lee and colleagues90 conducted a systematic review of use of Tai Chi for osteoarthritis. Authors conducted systematic searches on Medline, AMED, British Nursing Index, CINAHL, Embase, PsycINFO, The Cochrane Library 2007, Issue 2, the UK National Research Register, ClinicalTrials.gov, Korean medical databases, the Qigong and Energy database and Chinese medical databases (until June 2007). Hand searches included conference proceedings and the authors‘ own files. Five RCTs assessed the effectiveness of Tai Chi on pain of osteoarthritis. Two RCTs suggested significant pain reduction on VAS or Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) compared to routine treatment and an attention control program in knee osteoarthritis. Three RCTs did not report significant pain reduction on multiple pain sites. In a prospective, pretest-posttest clinical trial, Shen and colleagues91 examined the effects of Tai Chi exercise on gait kinematics, physical function, pain, and pain self-efficacy in elderly with knee osteoarthritis. After 6 weeks of Tai Chi exercise, knee pain was

significantly decreased (P = .002), whereas no change was observed in pain self-efficacy. Lee and Lee92 studied effects of Tai Chi exercise on pain and stiffness of knee joint in forty-six community-dwelling elderly subjects with osteoarthritis. The experimental group had significantly less pain (P = .008) and stiffness (P = .003) than the control group. Wang and colleagues93 discuss the challenges of designing an RCT with long-term follow up. Their RCT examines the effects of a 12-week Tai Chi program compared with an attention control (wellness education and stretching) on pain, functional capacity, psychosocial variables, joint proprioception, and health status in elderly people with knee osteoarthritis and is expected to be completed by July 2009. The challenges encountered by the authors included strategies for recruitment, avoidance of selection bias, the actual practice of Tai Chi, and the maximization of adherence and follow-up while conducting the clinical trial for the evaluation of the effectiveness of Tai Chi on knee osteoarthritis. Two studies examined comparative efficacy of hydrotherapy and Tai Chi in patients with osteoarthritis. Lee94 compared the effects of Tai Chi, aquatic exercise, and a self-help program in 50 patients. There were significant differences in joint pain (P = .000) and stiffness (P = .001) for both the Tai Chi and the aquatic exercise groups compared to the self-help group. In a larger RCT, Fransen and colleagues95 randomly allocated 152 older persons with chronic symptomatic hip or knee OA for 12 weeks to hydrotherapy classes, Tai Chi classes, or a waiting list control group. Outcomes were assessed 12 and 24 weeks after randomization and included pain and physical function (Western Ontario and McMaster Universities Osteoarthritis Index). At 12 weeks, compared with controls, participants allocated to hydrotherapy classes and Tai Chi classes demonstrated significant improvements for pain scores. All significant improvements were sustained at 24 weeks. Interestingly, class attendance was higher for hydrotherapy, with 81% attending at least half of the available 24 classes, compared with 61% for Tai Chi. Similarly, while demonstrating significant pain reduction in the Tai Chi group, the dropout rate in the study by Song and others96 was 41%. In contrast to the findings of Fransen and colleagues, Brismee and associates97 found that although 6 weeks of group Tai Chi followed by another 6 weeks of home Tai Chi training resulted in significant improvements in mean overall knee pain (P = .0078) and maximum knee pain (P = .0035) compared to controls, all improvements disappeared after “detraining” at 18 weeks. Several studies investigated using Tai Chi in pain associated with rheumatoid arthritis.

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Han and colleagues98 attempted to assess the effectiveness and safety of Tai Chi as a treatment for people with rheumatoid arthritis. These authors searched the Cochrane Controlled Trials Register, Medline, PEDro and CINAHL databases, the Chinese Biomedical Database and the Beijing Chinese Academy of Traditional Medicine. RCTs and controlled clinical trials examining the benefits and harms of exercise programs with Tai Chi instruction or incorporating principles of Tai Chi philosophy were selected for review and included four trials including 206 participants. Although the included studies did not assess the effects on patient-reported pain, the results suggest Tai Chi does not exacerbate symptoms of rheumatoid arthritis. Yocum and colleagues99 reviewed the role of exercise, education, and behavioral modification as alternative therapy for pain and stress in rheumatoid arthritis. Their analysis indicated that programs using alternative therapies such as Tai Chi in combination with traditional medications appear to be beneficial for patients with arthritis, and that these individuals appear to live better lives and may have better long-term outcomes[M8]. They argue that methods such as Tai Chi relieve stress and alter endocrine and immune system functions in ways that relieve rheumatoid arthritis pain. A systematic review of Medline, PubMed, AMED, British Nursing Index, CINAHL, Embase, PsycINFO, The Cochrane Library, the UK National Research Register and ClinicalTrials.gov, Korean medical databases, Qigong and Energy Medicine Database, and Chinese databases identified two RCTs that assessed pain outcomes in patients with rheumatoid arthritis who performed Tai Chi. The trials did not demonstrate effectiveness on pain reduction compared with education plus stretching exercise and usual activity control.100 Yet, in a controlled trial of 61 subjects with rheumatoid arthritis, Lee and Jeong101 found that pain and fatigue significantly decreased in the experimental group[M9]. Koh describes his personal experience with using Tai Chi for symptoms of ankylosing spondylitis that are unresponsive to conventional therapies.102 After 2½ years of daily practice the author felt less pain in addition to other positive results. However, pain returned if practice was neglected for as little as 1 week. There were also several studies examining effects of Tai Chi on pain in college students and the elderly. Wang and coworkers103,104 administered a 3-month intervention of Tai Chi exercise to college students, and multidimensional physical and mental health scores including bodily pain were assessed using the SF-36 health survey questionnaire before and after the intervention. Bodily pain improved significantly after Tai Chi exercise intervention. Reid and colleagues105 reviewed the evidence regarding self-management interventions for pain due to musculoskeletal disorders among older adults. After searching the Medline and Cumulative Index to Nursing and Allied Health Literature databases, authors identified 27 articles that evaluated programs including yoga, massage therapy, Tai Chi, and music therapy. Positive outcomes were found in 96% of the studies. Proportionate change in pain scores ranged from an increase of 18% to a reduction of 85% (median, 23% reduction). Generalizability issues identified included limited enrollment of ethnic minority elders, as well as nonethnic elders aged 80 and older. Another review, conducted by Morone and Greco,106 found limited support for meditation and Tai Chi for improving function or coping in older adults with low back pain or osteoarthritis.

Several studies included older adults, but did not analyze benefits by age. Tai Chi, yoga, hypnosis, and progressive muscle relaxation were significantly associated with pain reduction in these studies. Ross and others107 evaluated effects of Tai Chi exercise on 11 elderly women. Findings included significant improvement (P = .05) in pain perception as measured by the Visual Analog Scale. Ho and colleagues compared health-related quality of life in 140 elderly practicing Tai Chi and 560 age- and sex-matched control subjects taken from the general population.108 Authors found no significant difference in the bodily pain scales between Tai Chi and control groups. Despite these findings, in a larger study using similar design, Kin and associates109 found that when the 804 elderly participants were further subdivided in age cohorts, the 70- to 80-year old subjects practicing Tai Chi had significantly better bodily pain scores (P < .05) than the age- and sex-matched national average. Finally, in a fascinating study involving 112 healthy older adults aged 59 to 86, Irwin and colleagues110 set out to evaluate the effects of Tai Chi on resting and vaccine-stimulated levels of cell-mediated immunity (CMI) to varicella zoster virus (VZV) and on health functioning in older adults. In a prospective, RCT, the subjects were vaccinated with the live attenuated VZV vaccine licensed to prevent varicella. The Tai Chi group showed significant improvements in SF-36 scores for bodily pain, vitality, and mental health (P < .05). The benefits of Tai Chi are unclear but the risks are not. It is a safe form of physical and mental activity that health care practition­ ers should take into account when treating a patient with chronic pain.

Alexander Technique Alexander technique is a methodology for the treatment of chronic illness or conditions due to stress. Although it does not cure any of the conditions, Alexander technique does manage to make the condition less taxing on the afflicted individual. In general, the technique works through psychosensory education; the afflicted individuals are taught by teachers of Alexander technique to identify habits that may be the cause of unnecessary and extra discomfort. Interestingly, Alexander technique does not involve any exercises or forms of meditation; it is essentially a system of self-analysis and eventually, one of self-care.111 The origin of Alexander technique is rooted in the personal experiences of Frederick Matthias Alexander. Born in 1869, he eventually became a Shakespearian recitalist at age 19. However, he experienced recurring laryngitis. The medical help he sought was unable to identify the cause of his condition.112 One day, however, Alexander began to question how he used his voice. Eventually, realized that whenever he would go on stage, his body would produce an unconscious response; his body would tighten up. At first, he attempted to correct his problem by “standing straight,” but this only managed to worsen his condition. Alexander managed to overcome his problem by being consciously aware of himself while he spoke. He discovered that by doing so, he could release the tension in his body and be more relaxed while he spoke. The key to his method rests in the focus of the moment, or having active sensory awareness, rather than focusing on the product, the outcome of the moment.113 The notion of posture was also addressed by the Alexander technique. According to Alexander, the spine naturally lengthens as an individuals becomes aware of their own movements, thereby maximizing the comfort of the body. When an individual forces himself or herself to follow an idea of posture, the body cannot

Body Work and Movement Therapies  217

naturally assume it because of the mind’s influence. Therefore, Alexander believed that “poise”, a term associated with plasticity, would more be a more appropriate word than “posture”, a static word.114 In practice, the Alexander technique involves a one-to-one lesson between the student and the teacher, in which the teacher aids the student in identifying his or her own unwanted tensions and reactions, allowing the student to eventually develop self-care. The teachers of Alexander technique emphasize everyday activities, which include reading, sitting, lying down, and so on. By doing so, the student goes through each of the Alexander technique stages: “the means-whereby (conscious awareness in action) and nonendgaining (process over product), inhibition (nondoing, noninterference), and direction (carrying out clear intention to move).”115 The Alexander technique generally applies to individuals with neurologic and musculoskeletal problems. Typical afflictions and conditions that Alexander technique can help include pain management, chronic fatigue syndrome, disc herniation, sciatica, osteoporosis, stenosis, occupational injuries, and strains of musicians, dancers, computer workers, and singers.116 In Maher’s 2004 article117 analyzing scientific evidence for various physical treatments of low back pain, he groups the Alexander technique with other therapies of “unknown efficacy” (see Table 21-8) given the paucity of high-quality clinical trials evaluating it. Alexander technique has been shown to be effective when it is part of a multidisciplinary approach to chronic lower back pain.118 Elkayam and colleagues in Israel found significant reductions in pain after a 4-week program of back school, psychological intervention, chiropractic manipulation, Alexander technique, and acupuncture. Using the VAS, pain ratings dropped from a mean of 7.02 to 4.67 (P < .01) and was maintained for 6 months following treatment. Yet the researchers did not identify the contributions of the different modalities and, thus, no conclusions can be made about any of them individually. Researchers in the United Kingdom119 performed a systematic review of controlled, clinical trials evaluating the effectiveness of the Alexander technique. In their search of Medline, Embase, Amed, CSICOM, and Cochrane Library, as well as material from experts in the field, two trials were methodologically sound and clinically relevant. One of those addresses pain, an unpublished trial by Vickers of patients with chronic mechanical low back pain (Table 21-9). When compared to controls who received weekly self-help meetings, there seemed to be pain improvement in the experimental group at 3-month follow-up. However, more recently Little and colleagues120 reported the results of an RCT to determine the effectiveness of Alexander technique lessons, exercise, and massage for chronic and recurrent back pain. The 579 participants in the trial (average age 45 years) reported an average of 279 days of pain in the past year (SD 131). The participants were assigned to receive either normal care (control), 6 sessions of massage, or 6 or 24 lessons on the Alexander technique. Half of the patients in each of these groups also received a prescription for exercise from a doctor as well as behavioral counseling from a nurse (Table 21-10). At follow-up after 3 months, the patients in the massage and Alexander technique groups reported statistically significant fewer days with back pain in the previous month when compared with the control group (Table 21-11). The patients who received 24 sessions of Alexander technique had the greatest mean decrease in days with back pain with an average of 16 fewer days. The exercise prescription group also showed a modest effect, decreasing the number of days with pain in a month by 6.

Table 21-8  Summary of Efficacy of Physical Treatments for Chronic LBP Conclusion on Efficacy

Treatment Exercise

Effective: Large/­ Durable Effect

Effective: Small or Transient Effect

Unknown Efficacy

+

Laser

+

Massage

+

Spinal manipulation

+

Multi­ disciplinary ­rehabilitation

Ineffective

+

Hydrotherapy

+

Magnets

+

TENS

+

Traction

+

Ultrasound

+

Acupuncture

+

Back schools

+

Lumbar ­supports

+

Pilates

+

Beds/­ mattresses

+

Feldenkrais

+

Alexander technique

+

Craniosacral therapy

+

From Maher CG: Effective physical treatment for chronic low back pain. Orthop Clin North Am 2004;35:57-64.

In addition, at 1-year follow-up, the group who received 24 lessons in Alexander technique continued to have significantly fewer days with pain (a mean of 18 fewer days) (Table 21-12). The participants who had received 6 lessons on Alexander technique or massage also had significantly fewer days with pain (10 fewer and 7 fewer, respectively). At 1 year, however, the exercise group failed to show significantly fewer days with pain. This high-quality study gives strong support for the long-term benefits of the Alexander technique. The fact that those participants who received only six sessions still had nearly as few days of back pain as the group who received 24 sessions may indicate the powerful nature of this method. However, this is just one clinical trial and more need to be performed.

Body Awareness Therapy Basic body awareness therapy (BAT) is a method of increasing the quality of movement through an increase in body awareness. The Basic Body Awareness Therapy uses everyday activities such as

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218  Complementary and Alternative Medical Procedures

Table 21-9  Results of Unpublished Trial Evaluating Alexander Technique for Chronic Low Back Pain First Author (Year) Vickers (unpublished)

Design

Jadad Score

RCT with 3 parallel arms

3

Patients 91 patients with chronic mechanical low back pain (CMLBP)

Experimental Intervention

Control Intervention

20 biweekly AT sessions

(1) 10 weekly self-help meetings (2) No ­treatment

Outcome Measures

Main Results

Pain VAS raw score (RPS), disability score (DS), inappropriate pain behavior (IPB)

At post-test IPB and DS ­significantly improved relative to controls (P <.0001). At 3 mo only RPS was significantly ­better in the AT group; at 6 mo only DS; at 12 mo none of the o­utcomes favored AT

AT, Alexander technique; RCT, Randomized controlled trial; VAS, Visual analog scale. From Ernst E, Canter PH: The Alexander Technique: A systematic review of controlled clinical trials. Forsch Komplementarmed Klass Naturheilkd 2003;10:325-329.

Table 21-10  Trial Groups for Patients with Chronic or Recurrent Back Pain No Exercise

Exercise*

Normal care

Intervention

Group 1 (control)

Group 5

Therapeutic ­massage (six sessions)†

Group 2

Group 6

Alexander technique lessons (n = 6)‡

Group 3

Group 7

Alexander technique lessons (n = 24)§

Group 4

Group 8

*Doctor prescription and up to three sessions of behavioral counseling with practice nurse. Doctor exercise prescription was scheduled 6 wk into trial to allow groups 7 and 8 to have Alexander technique lessons before starting exercise but not to delay any further the start for group 5. †One session/wk for 6 wk. ‡Two lessons/wk for 2 wk, then one lesson/wk for 2 wk. §Twenty-two lessons over 5 mo, initially two lessons/wk for 6 wk, one lesson/wk for   6 wk, one lesson every 2 wk for 8 wk, and one revision lesson at 7 mo, and one at 9 mo. From Little P, Lewith G, Webley F, et al: Randomized controlled trial of Alexander technique lessons, exercise, and massage (ATEAM) for chronic and recurrent back pain. BMJ 2008;337:a884.

walking and standing but it can also incorporate a wide range of psychophysical practices including Yoga and Tai Chi Chuan. BAT is based on Jacques Dropsy’s movement system.121 The Feldenkrais method is a specific form of BAT that focuses on allowing people to move in more efficient ways. The Feldenkrais method was developed by Moshe Feldenkrais in response to a personal knee injury. Using his knowledge of athletics, Feldenkrais explored different forms of movement with his knee, learning to use the least painful method.122 Eventually, he learned to walk again without pain. Publishing his understanding of the process in Body and Mature Behavior and then again in a more refined manner in Awareness Through Motion, Feldenkrais eventually began to teach his method in classes in 1969. By the time of his death in 1984, Feldenkrais trained about 300 practitioners his method. The emphasis of the Feldenkrais method is to help afflicted individuals reduce their pain through an understanding of more efficient movement. The method applies not only to chronic physical conditions but also to mental conditions. In Body and Mature Behavior, Feldenkrais finds “successful action” as action that requires the least amount of exertion.123 An example of an exercise of the method includes shifting weight between the left and right side of the body, then becoming more complex with vertical and horizontal movement. Simplicity and working at one’s own comfort level are fundamental throughout the process. One

practitioner stated: “Because there were contrasting sensations in each side, my physical awareness increased…So automatic is goaloriented work that one doesn’t recognize effort, as such, until led to a heightened state of awareness where subtle energy differences can be perceived.” Several studies in Scandinavia have demonstrated the advantage of BAT over traditional physiotherapeutic treatment, especially when it is part of a multidisciplinary approach. One prospective, controlled, follow-up study by Grahn and colleagues at Lund University in Sweden124 investigated patients with prolonged musculoskeletal disorders (i.e., more than 6 months). The 122 patients in the rehabilitation group received BAT and cognitive and relaxation therapy for 4 weeks. Matched controls (114 patients) received traditional treatment within primary care, medical examination, advice, prescription of medicine, assessment of the need for sick leave, and a referral for physiotherapy. The rehabilitation group’s pain rating on the VAS improved from a mean of 67.5 to 59.4 after 6-month follow-up (P = .0005). Conversely, the control group did not show a significant improvement in pain rating at follow-up. A 2002 study by Gustafsson and colleagues,125 also in Sweden, studied 43 women with fibromyalgia or chronic, widespread pain who were nonrandomly assigned to receive either a multidisciplinary rehabilitation program including BAT or no therapy program. The experimental group did not demonstrate improvement of pain with BAT that was superior to the control group, although there were other benefits such as movement quality. BAT and Feldenkrais alone (not as part of a multimodal approach) have been compared to other physical therapies. In another Swedish study,126 78 patients with nonspecific musculoskeletal disorders were recruited consecutively over a period of 9 months. Physical complaints included headache, neck and shoulder pain, and back pain. Patients received 20 sessions of either Basic BAT, Feldenkrais or conventional physiotherapy (based on which health care district they presented to) over 4 to 5 months. Pain was assessed before treatment, at 6 months, and at 1 year by the 36-item Short Form Health Survey.127 All three groups had a significant decrease in bodily pain over time, but effect-size analysis indicated that Basic BAT and Feldenkrais may be more effective than conventional treatment. Basic BAT and Feldenkrais both had a large effect size (greater than 1.0), whereas conventional therapy had a small effect size (less than 0.5). Two different types of BAT, Basic BAT and Mensendieck, have been directly compared. This pilot study examined 20 female patients with fibromyalgia who were randomized to receive one of the two therapies for 20 weeks. At 18 months follow-up, the patients who received Mensendieck therapy improved more in terms of

Body Work and Movement Therapies  219

Table 21-11  Outcomes at 3 Months after Randomization. Values are Mean Differences Compared with Control Group (95% Confidence Intervals) and P Values, Unless Stated Otherwise

Outcomes

Mean (SC) ­Control ­(Alexander ­Technique ­Factor)*

Mean Difference Compared with Control, P Value

Massage

6 lessons in Alexander Technique

24 Lessons in Alexander Technique

Mean (SD) Control (Exercise ­Factor*)

Mean Difference Compared with Control: Exercise

Primary outcomes Roland disability score†(n = 469)

9.34 (4.76)

−1.96 (−0.74 to 3.18), P = .002

−1.71 (−2.95 to −0.47), P =.007

−2.91 (−4.16 to 1.66), P < .001

8.35 (4.75)

−0.90 (−1.76 to 0.04), P = .04

Median (95% CI) No. of days with back pain in past 4 wk (n = 405)‡

24 (21 to 27)

−13 (−18 to −8), P < .001

-11 (-16 to -6), P < .001

-16 (-21 to -11) P < .001

17 (15 to 19)

−6 (−9 to −3), P < .001

From Little P, Lewith G, Webley F, et al: Randomized controlled trial of Alexander technique lessons, exercise, and massage (ATEAM) for chronic and recurrent back pain. BMJ 2008;337:a884.

Table 21-12  Outcomes at 1 Year After Randomization: Mean Difference Compared with Control Group (95% Confidence Intervals) Unless Specified Otherwise

Outcomes

Mean (SC) ­ ontrol C ­(Alexander ­Technique ­Factor)*

Mean Difference Compared with Control, P Value

Massage

Six Lessons in ­Alexander Technique

24 Lessons in ­Alexander ­ Technique

Mean (SD) Control (Exercise ­Factor*)

Mean Difference ­Compared with Control: Exercise

Primary outcomes Roland disability score (n = 462)

8.07 (6.13)

−5.8 (−1.94 to 0.77), P =.399

−1.40 (−2.77 to −0.03), P = .045

−3.40 (−4.76 to −2.03), P < .001

7.54 (6.25)

−1.29 (−2.25 to −0.34),   P = .008

Median (95% CI)   No. of days with back pain in past 4 wk (n = 435)

21 (18 to 25)

−7 (−12 to −2), P = .004

−10 (−15 to −5), P < .001

−18 (−23 to −13), P < .001

13 (11 to 15)

−2 (−5 to 1), P = .233

From Little P, Lewith G, Webley F, et al: Randomized controlled trial of Alexander technique lessons, exercise, and massage (ATEAM) for chronic and recurrent back pain. BMJ 2008;337:a884.

symptom reduction and pain relief than those who received Basic BAT. For example, on the Arthritis Self-Efficacy Scale, one of the questionnaires administered to all participants, those who received Mensendieck rated their pain control 62/100 six months after therapy. Those who received basic BAT rated their pain control only 32/100 at this same point in time.128 Several cases of patients with chronic lower back pain who responded to the Feldenkrais method after failing a variety of traditional and nontraditional methods were reported by an Australian family physician.129 He photographically documented their changes in posture following treatment. However, he demonstrates only improved posture in his report, not an objective or subjective decrease in pain. One cannot assume that improved posture and body positioning necessarily relieves lower back pain. A 1977 Canadian study recruited participants from two retirement housing complexes in British Columbia. They received detailed health evaluations including measurement of height, weight, blood pressure, heart rate, flexibility, and number of body parts difficult to move or giving rise to pain. They were then assigned to receive a conventional exercise program, Feldenkrais exercises, or no exercise program over 6 weeks. Subsequent measurements failed to demonstrate any significant differences between groups. This study

was confounded by the fact that nearly 50% of the subjects dropped out or were unable to complete at least half the sessions.130 Given the equivocal data and dearth of research, a 2004 article by Maher131 evaluating various treatments for chronic lower back pain labeled Feldenkrais as being of “unknown efficacy.” According to the author, there is insufficient evidence for it to be considered by doctors or therapists for treating pain. A summary table from this article on the efficacy of physical treatments for chronic lower back pain is in Table 21-8. Overall, it seems that BAT, including Feldenkrais, can potentially improve pain and no studies so far indicate that it has negative effects. However, BAT needs to be further studied with larger, controlled trials before it is seriously considered an option by doctors for pain management. [M1]What did he do? [M2]How was pain measured? By how much (%) did it improve? [M3]Data? [M4]Data? By what % did pain decrease? [M5]What were results? [M6]More detail on data. But table of trials, maybe. [M7]What is the evidence? [M8]In terms of pain? [M9]data

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220  Complementary and Alternative Medical Procedures

REFERENCES  1. Snyder M, Lindquist R, eds. Complementary/Alternative Thera­ pies in Nursing. 5th ed. New York: Springer; 2006:108. http://site. ebrary.com/lib/nyulibrary/Doc?id=10171392&ppg=118.  2. Wainapel SF, Fast A, eds. Alternative medicine and rehabilitation: A guide for practitioners. New York: Demos Medical; 2002:139. http://site. ebrary.com/lib/nyulibrary/Doc?id=10118505&ppg=151.  3. Fishman http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505&ppg=152.  4. Cameron http://site.ebrary.com/lib/nyulibrary/Doc?id=10171392&ppg=119.  5. Fishman http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505&ppg=153.  6. Wilson RL. An introduction to yoga. AJN. 1976;76(2):261-263.  7. Wilson RL. An introduction to yoga. AJN. 1976;76(2):263.  8. Groessl EJ, Weingart KR, Aschbacher K, et al. Yoga for veterans with chronic low-back pain. J Altern Complement Med. 2008;14(9): 1123-1129.  9. Tekur P, Singphow C, Nagendra HR, Raghuram N. Effect of short-term intensive yoga program on pain, functional disability and spinal flexibility in chronic low back pain: A Randomized control study. J Altern Complement Med. 2008;14(6):637-644.   10. Kolasinski SL, Garfinkel M, Tsai AG, et al. Iyengar yoga for treating symptoms of osteoarthritis of the knees: A pilot study. J Altern Com­ plement Med. 2005;11:689-693.   11. Williams KA, Petronis J, Smith D, et al. Effect of Iyengar yoga therapy for chronic low back pain. Pain. 2005;115:107-117.   12. Melzack R. The short-form McGill Pain Questionnaire. Pain. 1987; 30:191-197.   13. Huskisson EC. Visual analogue scales. In: Melzack R, ed. Pain Mea­ surement and Assessment. New York: Raven Press; 1983:33-37.   14. Sherman KJ, Cherkin DC, Erro J, et al. Comparing yoga, exercise, and a self-care book for chronic low back pain. Ann Intern Med. 2005;143:849-856.   15. Da Silva GD, Lorenzi-Filho G, Lage LV. Effects of yoga and the addition of Tui Na in patients with fibromyalgia. J Altern Complement Med. 2007;13(10):1107–1013.   16. Morone NE, Greco CM. Mind-body interventions for chronic pain in older adults: A structured review. Pain Med. 2007;8:359-375.   17. John PJ, Sharma N, Sharma CM, et al. Effectiveness of yoga therapy in the treatment of migraine without aura: A randomized controlled trial. Headache. 2007;47:654-661.   18. Garfinkel MS, Singhal A, Katz WA, et al. Yoga-based intervention for carpal tunnel syndrome: A randomized trial. JAMA. 1998;280:1601-1603.   19. Michlovitz SL. Conservative interventions for carpal tunnel syndrome. J Orthop Sports Phys Ther. 2004;34:589-600.   20. Garfinkel MS, Schumacher HR Jr, Husain A, et al. Evaluation of a yoga based regimen for treatment of osteoarthritis of the hands. J Rheuma­ tol. 1994;21:2341-2343.   21. Carson JW, Carson KM, Porter LS, et al. Yoga for women with metastatic breast cancer: Results from a pilot study. J Pain Symptom Man­ age. 2007;33:331-341.   22. Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low back pain: A joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007;147:478-491.   23. “What Is Pilates?” http://www.pilates.com/BBAPP/V/pilates/index. html   24. “Pilates Origins.” http://www.pilates.com/BBAPP/V/pilates/origins-ofpilates.html   25. “Getting Started.”  http://www.pilates.com/BBAPP/V/pilates/gettingstarted.html   26. Maher CG. Effective physical treatment for chronic low back pain. Orthop Clin North Am. 2004;35(1):57-64.   27. La Touche R, Escalante K, Linares MT. Treating non-specific chronic low back pain through the Pilates method. J Bodyw Mov Ther. 2008;12:364-370.

  28. Verhagen AP, de Vet HC, de Bie RA, et al. The Delphi list: A criteria list for quality assessment of randomized clinical trials for conducting systematic reviews developed by Delphi consensus. J Clin Epidemiol. 1998;51(12):1235-1241.   29. Jadad AR, Moore RA, Carroll D, et al. Assessing the quality of reports of randomized clinical trials: Is blinding necessary? Control Clin Trials. 1996;17:1-12.   30. Donzelli S, Di Domenica E, Cova AM, et al. Two different techniques in the rehabilitation treatment of low back pain: A randomized controlled trial. Eura Medicophys. 2006;42:205-210.   31. Rydeard R, Leger A, Smith D. Pilates-based therapeutic exercise: Effect on subjects with nonspecific chronic low back pain and functional disability: A randomized controlled trial. J Orthop Sports Phys Ther. 2006;36:472-484.   32. Keays KS, Harris SR, Lucyshyn JM, et al. Effects of Pilates exercises on shoulder range of motion, pain, mood, and upper-extremity function in women living with breast cancer: A pilot study. Phys Ther. 2008;88:494-510.   33. Cleeland CS, Ryan KM. Pain assessment: Global use of the Brief Pain Inventory. Ann Acad Med Singapore. 1994;23:129-138.   34. Tan JC, Wainapel SF, eds. Alternative Medicine and Rehabilitation. A Guide for Practitioners. New York: Demos Medical; 2002:77. http:// site.ebrary.com/lib/nyulibrary/Doc?id=10118505&ppg=89.   35. Tan JC. http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505&ppg=90.   36. Snyder M. Complementary/alternative therapies in nursing. 5th ed. New York: Springer; 2006:288. http://site.ebrary.com/lib/nyulibrary/ Doc?id=10171392&ppg=291.   37. Sherman KJ, Cherkin DC, Deyo RA, et al. The diagnosis and treatment of chronic back pain by acupuncturists, chiropractors, and massage therapists. Clin J Pain. 2006;22(3):227-234.   38. Wells M, Sarna L, Cooley ME, et al. Use of complementary and alternative medicine therapies to control symptoms in women living with lung cancer. Cancer Nurs. 2007;30(1):45-55.   39. Wolsko PM, Eisenberg DM, Davis RB, et al. Patterns and perceptions of care for treatment of back and neck pain: Results of a national survey. Spine. 2003;28(3):292-297.   40. Brett KM, Keenan NL. Complementary and alternative medicine use among midlife women for reasons including menopause in the United States: 2002. Menopause. 2007;14(2):300-307.   41. Palinkas LA, Kabongo ML, San Diego Unified Practice Research in Family Medicine Network . The use of complementary and alternative medicine by primary care patients. A SURF*NET study. J Fam Pract. 2000;49(12):1121-1130.   42. Williamson AT, Fletcher PC, Dawson KA. Complementary and alternative medicine. Use in an older population. J Gerontol Nurs. 2003;29(5):20-28.   43. Drivdahl CE, Miser WF. The use of alternative health care by a family practice population. J Am Board Fam Pract. 1998;11(3):193-199.   44. Feinglass J, Lee C, Rogers M, et al. Complementary and alternative medicine use for arthritis pain in 2 Chicago community areas. Clin J Pain. 2007;23(9):744-749.   45. McCasland LD, Budiman-Mak E, Weaver FM, et al. Shoulder pain in the traumatically injured spinal cord patient: Evaluation of risk factors and function. JCR: J Clin Rheumatol. 2006;12(4):179-186.   46. Ernst E. Manual therapies for pain control: Chiropractic and massage. Clin J Pain. 2004;20(1):8-12.   47. Moyer CA, Rounds J, Hannum JW. A meta-analysis of massage therapy research. Psychol Bul. 2004;130(1):3-18.   48. Back C, Tam H, Lee E, Haraldsson B. The effects of employer-provided massage therapy on job satisfaction, workplace stress, and pain and discomfort. Holist Nurs Pract. 2009;23(1):19-31.   49. Cleeland CS, Ryan KM. Pain assessment: Global use of the Brief Pain Inventory. Ann Acad Med Singapore. 1994;23(2):129-138.   50. Trinh K, Graham N, Gross A, et al. Acupuncture for neck disorders. Spine. 2007;32(2):236-243.

Body Work and Movement Therapies  221   51. Ezzo J, Haraldsson BG, Gross AR, et al. Massage for mechanical neck disorders: A systematic review. Spine. 2007;32(3):353-362.   52. Cherkin DC, Sherman KJ, Deyo RA, et al. A review of the evidence for the effectiveness, safety, and cost of acupuncture, massage therapy, and spinal manipulation for back pain. Ann Intern Med. 2003;138(11):898-906.   53. Furlan AD, Brosseau L, Imamura M, et al. Massage for low-back pain: A systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine. 2002;27(17):1896-1910.   54. Wright A, Sluka KA. Nonpharmacological treatments for musculoskeletal pain. Clin J Pain. 2001;17(1):33-46.   55. Best TM, Hunter R, Wilcox A, Haq F. Effectiveness of sports massage for recovery of skeletal muscle from strenuous exercise. Clin J Sport Med. 2008;18(5):446-460.   56. Moraska A. Therapist education impacts the massage effect on postrace muscle recovery. Med Sci Sports Exerc. 2007;39(1):34-37.   57. Dryden T, Baskwill A, Preyde M. Massage therapy for the orthopaedic patient: A review. Orthop Nurs. 2004;23(5):327-332.   58. Bennell KL, Hinman RS, Metcalf BR, et al. Efficacy of physiotherapy management of knee joint osteoarthritis: A randomised, double blind, placebo controlled trial. Ann Rheum Dis. 2005;64(6):906-912.   59. Ferrell-Torry AT, Glick OJ. The use of therapeutic massage as a nursing intervention to modify anxiety and the perception of cancer pain. Cancer Nurs. 1993;16(2):93-101.   60. Grealish L, Lomasney A, Whiteman B. Foot massage. A nursing intervention to modify the distressing symptoms of pain and nausea in patients hospitalized with cancer. Cancer Nurs. 2000; 23(3):237-243.   61. Currin J, Meister EA. A hospital-based intervention using massage to reduce distress among oncology patients. Cancer Nurs. 2008;31(3): 214-221.   62. Jane SW, Wilkie DJ, Gallucci BD, Beaton RD. Systematic review of massage intervention for adult patients with cancer: A methodological perspective. Cancer Nurs. 2008;31(6):E24-E35.   63. Williams PD, Schmideskamp J, Ridder EL, Williams AR. Symptom monitoring and dependent care during cancer treatment in children: Pilot study. Cancer Nurs. 2006;29(3):188-197.   64. Simkin PP, O’hara M. Nonpharmacologic relief of pain during labor: Systematic reviews of five methods. Am J Obstet Gynecol. 2002;186 (5 Suppl Nature):S131-S159.   65. Chang MY, Chen CH, Huang KF. A comparison of massage effects on labor pain using the McGill Pain Questionnaire. J Nurs Res. 2006;14(3):190-197.   66. Tzeng YL, Su TJ. Low back pain during labor and related factors. J Nurs Res. 2008;16(3):231-241.   67. Stamp G, Kruzins G, Crowther C. Perineal massage in labour and prevention of perineal trauma: randomised controlled trial. BMJ. 2001;322(7297):1277-1280.   68. Bellieni CV, Bagnoli F, Perrone S, et al. Effect of multisensory stimulation on analgesia in term neonates: A randomized controlled trial. Pediatr Res. 2002;51(4):460-463.   69. Bellieni CV, Cordelli DM, Marchi S, et al. Sensorial saturation for neonatal analgesia. Clin J Pain. 2007;23(3):219-221.   70. Forchuk C, Baruth P, Prendergast M, et al. Postoperative arm massage: A support for women with lymph node dissection. Cancer Nurs. 2004;27(1):25-33.   71. Anderson PG, Cutshall SM. Massage therapy: A comfort intervention for cardiac surgery patients. Clin Nurse Spec. 2007;21(3):161-165.   72. Carrieri-Kohlman V, Lindsey A, West C. Pathophysiological Pheno­ mena in Nursing, Human Responses to Illness. St. Louis: Saunders; 2003.   73. Erdogmus CB, Resch KL, Sabitzer R, et al. Physiotherapy-based rehabilitation following disc herniation operation: Results of a randomized clinical trial. Spine. 2007;32(19):2041-2049.   74. Mitchinson AR, Kim HM, Rosenberg JM, et al. Acute postoperative pain management using massage as an adjuvant therapy: A randomized trial. Arch Surg. 2007;142(12):1158-1167.

  75. Field T, Peck M, Krugman S, et al. Burn injuries benefit from massage therapy. J Burn Care Rehabil. 1998;19(3):241-244.   76. Gallagher G, Rae CP, Kinsella J. Treatment of pain in severe burns. Am J Clin Dermatol. 2000;1(6):329-335.   77. Hernandez-Reif M, Field T, Largie S, et al. Childrens‘ distress during burn treatment is reduced by massage therapy. J Burn Care Rehabil. 2001;22(2):191-195.   78. Schneider JC, Harris NL, El Shami A, et al. A descriptive review of neuropathic-like pain after burn injury. J Burn Care Res. 2006;27(4):524-528.   79. KM, Snyder M. Complementary/Alternative Therapies in Nursing. 5th ed. New York: Springer; 2006:313. http://site.ebrary.com/lib/ nyulibrary/Doc?id=10171392&ppg=316.   80. Wolf SL, O’Grady MJ, Xu T, et al. eds. Alternative Medicine and Reha­ bilitation: A Guide for Practitioners. New York: Demos Medical; 2002. http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505&ppg=111.   81. Morton WS, Lewis CM. China: Its History and Culture. Blacklick, OH: McGraw-Hill; 2004:38. http://site.ebrary.com/lib/nyulibrary/Doc?id= 10083588&ppg=66.   82. Morton p 39. http://site.ebrary.com/lib/nyulibrary/Doc?id=10083588 &ppg=67.   83. Wolf 100. http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505& ppg=112.   84. Wolf 102. http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505& ppg=114.   85. Wolf 103. http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505& ppg=115.   86. Klein PJ, Adams WD. Comprehensive therapeutic benefits of Taiji: A critical review. Am J Phys Med Rehabil. 2004;83(9):735-745.   87. Wahbeh H, Elsas SM, Oken BS. Mind-body interventions: Applications in neurology. Neurology. 2008;70(24):2321-2328.   88. Chen KM, Snyder M. A research-based use of Tai Chi/movement therapy as a nursing intervention. J Holist Nurs. 1999;17(3): 267-279.   89. Siu AM, Chan CC, Poon PK, et al. Evaluation of the chronic disease self-management program in a Chinese population. Patient Educ Couns. 2007;65(1):42-50.   90. Lee MS, Pittler MH, Ernst E. Tai chi for osteoarthritis: A systematic review. Clin Rheumatol. 2008;27(2):211-218.   91. Shen CL, James CR, Chyu MC, et al. Effects of Tai Chi on gait kinematics, physical function, and pain in elderly with knee osteoarthritis—a pilot study. Am J Chin Med. 2008;36(2):219-232.   92. Lee HY, Lee KJ. Effects of Tai Chi exercise in elderly with knee osteoarthritis [Article in Korean] Taehan Kanho Hakhoe Chi. 2008;38(1):11-18.   93. Wang C, Schmid CH, Hibberd PL, et al. Tai Chi for treating knee osteoarthritis: Designing a long-term follow up randomized controlled trial. BMC Musculoskel Dis. 2008;9:108.   94. Lee HY. Comparison of effects among Tai-Chi exercise, aquatic exercise, and a self-help program for patients with knee osteoarthritis [Article in Korean] Taehan Kanho Hakhoe Chi. 2006;36(3):571-580.   95. Fransen M, Nairn L, Winstanley J, et al. Physical activity for osteoarthritis management: A randomized controlled clinical trial evaluating hydrotherapy or Tai Chi classes. Arthritis Rheum. 2007;57(3): 407-414.   96. Song R, Lee EO, Lam P, et al. Effects of a Sun-style Tai Chi exercise on arthritic symptoms, motivation and the performance of health behaviors in women with osteoarthritis. Taehan Kanho Hakhoe Chi. 2007;37(2):249-256.   97. Brismee JM, Paige RL, Chyu MC, et al. Group and home-based tai chi in elderly subjects with knee osteoarthritis: A randomized controlled trial. Clin Rehabil. 2007;21(2):99-111.   98. Han A, Robinson V, Judd M, et al. Tai chi for treating rheumatoid arthritis. Cochrane Database Syst Rev. 2004(3):CD004849.   99. Yocum DE, Castro WL, Cornett M. Exercise, education, and behavioral modification as alternative therapy for pain and stress in rheumatic ­disease. Rheum Dis Clin North Am. 2000;26(1):145-159:x–xi.

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222  Complementary and Alternative Medical Procedures 100. Lee MS, Pittler MH, Ernst E. Tai chi for rheumatoid arthritis: Systematic review. Rheumatology. 2007;46(11):1648-1651. 101. Lee KY, Jeong OY. The effect of Tai Chi movement in patients with rheumatoid arthritis [Article in Korean] Taehan Kanho Hakhoe Chi. 2006;36(2):278-285. 102. Koh TC. Tai Chi and ankylosing spondylitis—a personal experience. Am J Chin Med. 1982;10(1-4):59-61. 103. Wang YT, Taylor L, Pearl M, Chang LS. Effects of Tai Chi exercise on physical and mental health of college students. Am J Chin Med. 2004;32(3):453-459. 104. Wang Y. Tai Chi exercise and the improvement of mental and physical health among college students. Med Sport Sci. 2008;52:135-145. 105. Reid MC, Papaleontiou M, Ong A, et al. Self-management strategies to reduce pain and improve function among older adults in community settings: A review of the evidence. Pain Med. 2008;9(4):409-424. 106. Morone NE, Greco CM. Mind-body interventions for chronic pain in older adults: A structured review. Pain Med. 2007;8(4):359-375. 107. Ross MC, Bohannon AS, Davis DC, Gurchiek L. The effects of a shortterm exercise program on movement, pain, and mood in the elderly. Results of a pilot study. J Holist Nurs. 1999;17(2):139-147. 108. Ho TJ, Liang WM, Lien CH, et al. Health-related quality of life in the elderly practicing T’ai Chi Chuan. J Altern Complement Med. 2007;13(10):1077-1083. 109. Kin S, Toba K, Orimo H. Health-related quality of life (HRQOL) in older people practicing Tai Chi—comparison of the HRQOL with the national standards for age-matched controls [Article in Japanese]. Nippon Ronen Igakkai Zasshi. 2007 May;44(3):339-344. 110. Irwin MR, Olmstead R, Oxman MN. Augmenting immune responses to varicella zoster virus in older adults: A randomized, controlled trial of Tai Chi. J Am Geriatr Soc. 2007;55(4):511-517. 111. Batson G, Wainapel SF, eds. Alternative Medicine and Rehabilitation: A Guide for Practitioners. New York: Demos Medical; 2002: p175. http:// site.ebrary.com/lib/nyulibrary/Doc?id=10118505&ppg=187. http://site. ebrary.com/lib/nyulibrary/Doc?id=10118505&ppg=187. 112. Batson 176. http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505& ppg=188 113. Batson 177. http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505& ppg=189 114. Batson 178. http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505& ppg=190 115. Batson 179. http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505& ppg=191 116. Batson 176. http://site.ebrary.com/lib/nyulibrary/Doc?id=10118505& ppg=188

117. Maher CG. Effective physical treatment for chronic low back pain. Orthop Clin North Am. 2004;35:57. 118. Elkayam O, Ben Itzhak S, Avrahami E, et al. Multidisciplinary approach to chronic back pain: prognostic elements of the outcome. Clin Exp Rheumatol. 1996;14:281-288. 119. Ernst E, Canter PH. The Alexander technique: A systematic review of controlled clinical trials. Forsch Komplementarmed Klass Naturheilkd. 2003;10:325-329. 120. Little P, Lewith G, Webley F, et al. Randomised controlled trial of Alexander technique lessons, exercise, and massage (ATEAM) for chronic and recurrent back pain. BMJ. 2008;337:A884. 121. “Basic Body Awareness Therapy.” http://www.paramedisch.org/englishcourses/124-basic-body-awareness-therapy. 122. Strauch R: An overview of the Feldenkrais Method. Choices in Health Care: A Resource Guide to Contemporary Medicine and Therapy. Adriana Elmes (ed): in press. 1. 123. Linklater K. The Body Training of Moshe Feldenkrais. The Drama Review: TDR. 1972;16(1):24. 124. Grahn B, Ekdahl C, Borgquist L. Effects of a multidisciplinary rehabilitation programme on health-related quality of life in patients with prolonged musculoskeletal disorders: A 6-month follow-up of a prospective controlled study. Disabil Rehabil. 1998;20:285-297. 125. Gustafsson M, Ekholm J, Broman L. Effects of a multiprofessional rehabilitation programme for patients with fibromyalgia syndrome. J Rehabil Med. 2002;34:119-127. 126. Malmgren-Olsson EB, Branholm IB. A comparison between three physiotherapy approaches with regard to health-related factors in patients with non-specific musculoskeletal disorders. Dishabil Reha­ bil. 2002;24:308-317. 127. Sullivan M, Karlsson J. The Swedish SF-36 Health Survey I. Evaluation of data quality, scaling assumptions, reliability and construct validity across general populations in Sweden. Soc Sci Med. 1995;41:1349-1358. 128. Kendall SA, Brolin-Magnusson K, Sören B, et al. A pilot study of body awareness programs in the treatment of fibromyalgia syndrome. Arthritis Care Res. 2000;13:304-311. 129. Lake B. Acute back pain. Treatment by the application of Feldenkrais principles. Aust Fam Physician. 1985;14(11):1175-1178. 130. Gutman GM, Herbert CP, Brown SR. Feldenkrais versus conventional exercises for the elderly. J Gerontol. 1977;32(5):562-572. 131. Maher CG. Effective physical treatment for chronic low back pain. Orthop Clin North Am. 2004;35(1):57-64.

Mind Body Therapies and ­Posttraumatic Stress ­Disorder

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C. Norman Shealy, MD, PhD

Posttraumatic stress disorder (PTSD) is a common problem and its incidence has increased by the wars in Iraq and Afghanistan. Despite this recent increase in PTSD, the importance of stress in both physical and emotional disease has been emphasized for the past century. This chapter provides an overview of the history, common features, and effective body mind therapeutic approaches to PTSD.

Post Traumatic Stress Disorder: An Overview Discussions of the whole psychological concept of post traumatic stress disorder began when veterans returned from the Vietnam War. However, Sir William Osler, the Father of American Medicine, in his book, Aequanimitas,1 talked one hundred years ago about ordinary illnesses being due to the stress and strain of daily life. Hans Selye later brought to our attention the fact that virtually all illness is the result of stress.2 Indeed, having worked with over 30,000 individuals who had failed conventional medicine, many of them with chronic pain and all of them with chronic depression, it is my impression that virtually all illnesses are ultimately the result of unresolved stress, which frequently began in childhood. In other words post traumatic stress appears to be the root cause of illness. Situations that were perceived as either childhood abuse or abandonment impact an individual for life. Abuse tends to cause anger and abandonment leads to depression in adulthood. The extent of anger or depression varies significantly among individuals. Posttraumatic stress disorder is generally considered a more serious reaction that can occur almost instantly after major trauma or disaster. The most striking features of PTSD are flashbacks, recurrent memories and reliving of specific traumatic experiences. These same features appear to be in most patients with chronic depression or anxiety. These individuals can have rapidly developing emotional outbursts and often extremely bizarre behavior sometimes leading to rampages of murder or suicide. Indeed, it is these extremes that are the sine qua non of PTSD. If we look at the number of symptoms that are often part of posttraumatic stress disorder, they include3: Body aches and pains Bowel problems ll Difficulty with concentration ll Confusion ll Depression ll Difficulty relating to others ll ll

Fatigue Fearfulness ll Guilt ll Headache ll Irritability or anger ll Memory loss ll Nightmares ll Overeating or loss of appetite ll Sadness ll Skin disorders ll Sleeplessness or excessive sleeping ll Substance abuse and alcoholism ll Vomiting ll ll

PTSD Diagnosis The difficulty in establishing the diagnosis of PTSD has led to the development of a PTSD checklist (PCL). This checklist was developed from a population of 40 motor vehicle accident victims and sexual assault victims.4 The Iraq and Afghanistan wars have led to a striking increase in the number of soldiers diagnosed with PTSD. As one might expect, not everyone exposed to what appears to be the same intensity of trauma develops posttraumatic stress disorder. In one small study, 51 individuals who suffered a physical injury due to a traumatic event were assessed 1 week and 6 months after the trauma. Only 13 of these 51 (25.5%) met the posttraumatic stress disorder diagnostic criteria at follow-up. Those who did develop PTSD, had “higher levels of peritraumatic disassociation and more severe depression, anxiety, and intrusive symptoms” at the 1 week assessment. This peritraumatic disassociation at that initial week was a major factor in whether they later developed PTSD.5 In another study of 72 female rape victims versus 86 female victims of nonsexual assault, there were two patterns of posttraumatic symptoms, one being characterized as posttraumatic stress disorder and the second as a phobic reaction.6 Positron emission tomography (PET) has allowed perhaps the most clinically relevant view of brain function in PTSD. In 16 women with histories of childhood sexual abuse, 8 had current PTSD and 8 did not. When asked to recall or mentally recreate a traumatic event, both groups exhibited regional cerebral blood flow increases in the orbital frontal cortex in the anterior temporal poles. However, those with PTSD had a much greater increase in cerebral blood flow in those areas and those without PTSD had a greater decrease in cerebral blood flow in the left inferior frontal cortex. 223

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The non-PTSD had greater increases in the anterior cingulate gyri.7 Single photon emission computed tomography (SPECT) scans also have offered some insights into the physiologic changes apparent in PTSD patients. Fourteen veterans with PTSD, 11 combat control subjects and 14 normal subjects were all studied with the SPECT scans in sessions at least 48 hours apart. In one exposure, the individuals experienced white noise and in the other, they experienced exposure to combat sounds. Activation in all three groups occurred in the anterior, cingulate, and middle prefrontal gyri but activation in the region of the left amygdala and nucleus accumbens was found only in PTSD patients. Deactivation was found in all three groups in the left retrosplenic region.8 It appears that the PTSD individuals have regional differences in brain activity, at least during recall of their trauma. As one might expect, those individuals diagnosed with PTSD have a high incidence (80%) of having at least one other comorbid psychiatric diagnosis.9 It may be that the total lifelong cumulative stress to which individuals have been adversely subjected earlier in life predisposes them to PTSD. In one study of 131 Vietnam male veterans who had taken the Minnesota Multiphasic Personality Inventory (MMPI) in college had readings that were within the normal range, but no one scale predicted the development of stress from combat exposure. Hypochondriasis, psychopathic deviant, masculine femininity, and paranoia scales predicted PTSD symptoms, as did depression, hypomania, and social introversion and these effects were dominant despite the degree of combat exposure. The conclusion is similar to individuals in general. “Pre-military personality can affect vulnerability to lifetime PTSD symptoms in men exposed to combat.” This is thought to be true in individuals exposed to any trauma.10 In the author’s experience treating thousands of patients with chronic pain that failed all conventional therapy, at least 75% had elevations on depression, hypochondriasis, and hysteria, and an additional 15% had elevations on psychopathic deviant, masculine femininity, and paranoia.11 The most intense problem is the pattern of replaying many past traumatic events. Many of them can never remember a happy event from childhood. The main difference in these individuals and those with PTSD is that the chronic pain and depressed patients do not have the erratic episodes of intense emotional behavior. They are more passive. Finally, there has been an attempt to evaluate the role of shame, anger, and childhood abuse in victims of violent crime. One hundred fifty-seven victims of violent crime were interviewed 1 month after the crime and 6 months later. It was found that shame and anger were the only independent predictors of PTSD at 1 month and shame was the only independent predictor of PTSD at 6 months. The authors conclude that both shame and anger play important roles in the development of at least crime-related PTSD and that shame is the perpetuator in the subsequent course of symptoms.12 Another study supports the thesis that it is the childhood background that may determine one’s propensity to develop PTSD. In a telephone interview survey of 4023 adolescents aged 12 to 17 years, 16% of boys and 19% of girls met the criteria for at least one diagnosis of either PTSD, major depressive episode (MDE), or substance abuse/dependence (SA/D). The 6-month PTSD prevalence was 3.7% for boys at 6 months and 3% for girls, whereas, that of MDE was 7.4% for boys and 13.9% for girls. In the 12-month SA/D, prevalence was 8.2% for boys and 6.2% for girls. PTSD was more likely to be a comorbid condition than was MDE or SA/D. These results generally support the hypothesis that exposure to interpersonal violence (i.e., physical assault, sexual assault, or witnessed violence) increases the risk of the development of these major psychiatric disorders.13

Hans Eysenck’s Work on Anger and Depression The work of Hans Eysenck explores two other aspects of childhood emotional reaction and resultant lifelong depression and/or lifelong anger. He and colleagues studied over 13,000 adults over a 20-year period. Initially psychometric testing revealed the following four primary types of individuals: Lifelong hopelessness. Individuals who craved love and had felt abandoned ll Lifelong anger. Individuals who felt abused and carried a grudge ll Both lifelong depression and anger ll Autonomous individuals. These are well adjusted individuals who would probably be considered self-actualized. Essentially they say, “Happiness is an inside job. No one else can make me happy or unhappy.” ll

Eysenck discovered over two decades that approximately 75% of the individuals who died of cancer were the lifelong hopeless, 15% were angry, and 9% were both. Only 0.8% of those who died of cancer were autonomous. Additionally, approximately 75% of those who died of heart disease were lifelong angry, 15% were lifelong depressed, and 9% were lifelong both. Overall, the vast majority of the individuals who died in only twenty years were chronically angry, depressed, or both.14 These findings have significant implications for PTSD patients, who suffer even more intense anger, depression, or both.

Electromagnetic Dysthymia and PTSD Whatever the circumstances that predispose an individual to posttraumatic stress disorder, treatment for this particular difficult problem is primarily one for the field of mind-body medicine. Veterans have a high incidence of traumatic physical injury as well as psychological trauma. Thus, pain is common as a comorbid condition in these PTSD patients. In general, pain should always be treated when possible with appropriate correction of the physical or physiological cause. When such treatment does not lead to resolution of the pain within 6 months, it becomes a chronic pain syndrome. In the chronic pain syndrome, one should always consider procedures such as transcutaneous electrical nerve stimulation, acupuncture, physical exercise, and massage. In the author’s experience in working with more than 30,000 chronic pain patients, the most important long-term success have been achieved when these procedures are integrated with mind-body medicine. Many of these chronic pain patients fall into the category known as electromagnetic dysthymia. It is thought that these individual’s have brains with erratic electrical systems. Individuals with this disorder have the following characteristics15: A focus of excess electrical activity in one area of the brain. It is in the right frontal cortex 60% of the time, but it may be located in any area. ll A failed response to photostimulation. When presented with flashing lights at 10 Hz, they may have an increase in 3-cycle or 30-cycle activity, but not 10-cycle activity. ll A deficiency in one to seven essential amino acids, the building blocks for various neurochemicals. Deficiencies in taurine, an amino acid that regulates electrical charge on nerve cells, are found in 80%. ll A deficiency (100% of patients) in intracellular magnesium, which also regulates cell membrane potential. ll

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A wide spectrum of essential neurochemical abnormalities, especially norepinephrine, serotonin, melatonin, beta endorphin, and cholinesterase. ll A low or deficient levels (always found) of DHEA (dehydroepiandrosterone). ll An elevated production of cortisol. ll

It is the author’s experience that PTSD patients have these abnormalities.

Mind Body Therapies and PTSD Mind Body Medicine: History and Overview Today’s concept of mind body medicine evolved in the early 1970s from the humanistic psychology movement. Contributors to this movement included early biofeedback work by Dr. Elmer Green and his wife, Alyce, and the meditation and relaxation studies of Dr. Herb Benson. As early as 1964, Dr. George Solomon had begun his work on psychoimmunology, but the concept did not take off until Dr. Robert Ader expanded this work to the concept of psychoneuroimmunology in 1970.16,17 It was the discovery of endorphins and the work of Dr. Candace Pert that laid a solid chemical foundation for the concept.18 Mind-body medicine is a term that demonstrates physical, chemical, mental, and spiritual interconnectedness, and currently encompasses a wide variety of techniques. These include biofeedback, relaxation training, autogenic training, psychosynthesis, meditation, guided imagery, spiritual healing, prayer, Logotherapy, Gestalt therapy, and many other short-term psychotherapeutic interventions. Mesmerism itself was the first major development in the pre-modern prelude to today’s mind-body medicine. In the early 20th century, Emile Coue emphasized that “imagination” always wins in a conflict between “imagination and will.” Coue was famous for his statement, “Every day in every way I am getting better and better.” This statement was reported to cure thousands of people.19 The “separation” of mind and body is often said to have originated with Rene Descartes. Prior to his contributions, medicine, science, philosophy, and spirituality were commonly considered aspects of the whole person. With his influence in the 1600s, the separation of mind and body occurred—with mind being the purview of religion and metaphysics and body being the purview of science and medicine. In the late 18th century, Anton Mesmer began the trend to reexamine the connection of body and mind. Although rejected by most of his contemporaries, Mesmer’s work, said by Benjamin Franklin to be only a suggestion of the effect of the mind, spawned the concept of hypnosis, which was introduced by James Braid and James Eisdale after Dr. John Elliotson demonstrated in the 1840s that surgery could be performed on mesmerized patients. In 1872, Dr. Daniel Hack Tuke published the first major treatise on mind-body medicine in London. Tuke emphasized that the mind acts on the body through intellect, emotions, and volition. He considered that special and general sensations were influenced by mind, intellect, and volition, so he excluded these from his discussion. Conversely, he quotes Unser, who in 1771 wrote, “Expectation of the action of a remedy often causes us to experience its operation beforehand. This is also one of the earliest statements of the ­placebo effect.

John Hunter, of syphilis fame, had observed ‘mesmeric magnetism’ and came to the conclusion that “attention and expectation played a major role” in outcomes. James Braid took mesmerism to its more rational explanation, hypnosis. Hypnosis was highly controversial for more than 100 years, but led to the beginning of modern psychiatry. Sigmund Freud is said to have been such a poor hypnotist that he retreated to psychoanalysis. Jan Smuts, former Prime Minister of South Africa, wrote in the 1920s the most elegant integration of all aspects of science, philosophy, and psychology in his book, Holism and Evolution. This was essentially the foundation of what is now termed Holistics. William James discussed ‘mind cures’ extensively in his landmark book, The Varieties of Religious Experience, perhaps still the most in-depth study of religion and spirituality.

Relaxation for Stress Illnesses In 1929, Dr. Edmund Jacobsen published his landmark book, Progressive Relaxation, in which he demonstrated physiologic homeostasis with his practical technique of focused systematic muscle contraction and relaxation. He demonstrated that 80% of patients with “psychosomatic illness” were cured with this approach. It was never embraced by the medical profession. In 1912, Dr. J.H. Schultz of Germany had begun a specific form of self-hypnosis called autogenic training. His first book was published in 1932. By 1969, the six volumes on autogenic therapy were published by Schultz and Luthe.20 With some 2800 scientific references, they reported that 80% of “psychosomatic” illnesses were adequately treated with autogenic training. Additionally, athletes, business people, and students who practiced autogenic training markedly improved performance. Dr. Hans Selye demonstrated in the first half of the twentieth century the major effect of stress on health in general and maladaptation to stress as the basis of most disease. He emphasized the physiologic similarities of physical, chemical, and emotional stress. In 1954, the American Society of Psychosomatic Medicine was founded. It was, and remains, primarily a psychiatrically oriented concept. Unfortunately, the term psychosomatic, which should be called mind-body, has been considered by most patients and physicians to mean “all in the head.” Stress medicine would be a preferred term. Meanwhile the term placebo, which has been the standard since the beginning of modern scientific medicine, has been used and abused and is poorly understood by physicians and the public. The majority of drugs are only a few percent better than placebo, which in most controlled studies averages 35% efficacy. Few drugs are 70% efficacious. In the 1960s, Dr. Abraham Maslow and Dr. Carl Rogers began the reintegration of spirit and mind, founding humanistic psychology. Dr. Roberto Assagioli meanwhile had integrated all of his concepts, as well as Carl Jung’s concepts of symbology, into his technique of psychosynthesis. In 1970, Dr. Elmer Green and his wife, Alyce, introduced the concept of autogenic feedback training which has since become the foundation for biofeedback training. Their earliest work demonstrated that 84% of migraineurs and 80% of patients with hypertension were remarkably improved and adequately controlled with temperature biofeedback training. Since that time, it has been demonstrated that most physiologic responses, which can be measured and fed back to the patient visually or audibly, are capable of being brought under voluntary control.21 In the 1970s, Dr. Herbert Benson first reported on the physiologic homeostatic benefits of transcendental meditation and later

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recognized that the basic benefit was deep relaxation, soon to become known as the “relaxation response.” Benson’s work replicated what Jacobson had shown 50 years earlier. Most striking was Benson’s demonstration that individuals who performed 20 minutes of deep relaxation twice a day had a 50% decrease of catecholamine production and insulin requirement for the entire 24-hour period. In the early 1980s, George Solomon became one of the leading proponents of psychoneuroimmunology, which has provided the greatest evidence of the complete interconnectedness of body, mind, and attitude. Most remarkable is the finding that virtually every neurochemical produced in the brain is also produced in white blood cells and usually in the intestines. To some extent, the field of psychoneuroimmunology has suggested that the “mind” is part of every cell. Dr. Candyce Pert’s discovery of beta-endorphin, the natural opioid, was the first major step in demonstrating what Buryl Payne had introduced in Getting There Without Drugs in the 1970s. It now appears that the mind can produce a wide variety of mind-altering chemicals, ranging from anandamide to neurotensin with analgesic, neuroleptic, and hallucinogenic effects. Ultimately, mind-body medicine is the foundation for virtually all complementary and alternative medicine modalities.

Major Clinical Applications of Mind-Body Medicine The numerous, diverse mind-body therapies have been reported to be effective in pain control, migraine, rheumatoid arthritis, attention deficit hyperactivity disorder (ADHD), epilepsy, hypertension, peptic ulcer, anxiety, depression, PTSD, and diabetes. For example, 84% of migraineurs can control their headaches when they learn temperature control of the index finger, the least difficult biofeedback technique. In many chronic disorders, mind-body medicine is the approach of choice in stress illnesses and at the very least, is a major adjunct even when pharmaceuticals are necessary. Evidencebased approaches include relaxation for gastroesophageal reflux disease (GERD), hypnosis for irritable bowel syndrome, biofeedback and guided imagery for headaches, meditation and guided imagery for pain, and prayer for coronary artery disease. The most complex stress disorders include fibromyalgia, chronic fatigue, and posttraumatic stress disorder.. These patients fit into the syndrome earlier discussed as electromagnetic dysthymia (EMD).

Electromagnetic Dysthymia EMD is a generalized disorder of chronic fatigue, anxiety, depression, and a weakened immune system.22 In severe cases it would be called posttraumatic stress disorder. EMD is often misdiagnosed and goes under the rubric of environmental allergies, candidiasis, chronic fatigue, ME (myalgic encephalitis) in the United Kingdom, or RED syndrome (RNase-L defect). These problems in the author’s experience are associated with deficiency in DHEA, magnesium, and essential amino acids, especially tryptophan and taurine. Most significantly, depressed patients, even those without PTSD, appear to have the following: Magnesium deficiency Deficiency of one to seven essential amino acids, especially taurine ll Low or deficient DHEA ll Excess or deficient levels of norepinephrine, melatonin, serotonin, beta endorphin and/or cholinesterase ll ll

Abnormal computerized EEGs or brain maps with asymmetry. Most often there is excess activity in the right frontal area, but it may be in any lobe of the brain. ll Failure to respond appropriately to photostimulation. For example, instead of increasing 10 cycle photostimulation when presented, they may respond with 2 Hz or 20 Hz. ll

Treatment Protocol for EMD and PTSD In general, at least 85% of patients with these disorders improve with the following protocols: Transcranial stimulation with the Liss Cranial Electrical Stimulator (CES), applied 40 to 60 minutes each morning. Liss output is 1 to 2 milliamps of current at 15,000 Hz, modulated 15 and 500 Hz. Used alone it brings 50% of patients out of depression within 2 weeks. It is useful also in anxiety, insomnia, and jet lag. ll Photostimulation at 1 to 7 Hz. The Shealy RelaxMate has been used in more than 30,000 chronically depressed patients who also suffer from anxiety. Used alone, it helps 58% of depressed patients. When combined with the Liss, 85% of more than 30,000 chronically depressed patients have been improved, without drugs. ll Magnesium chloride—for the most rapid improvement, 2 g magnesium chloride daily for 10 days, given in 500 mL IV fluid with 2 g of vitamin C, 1 mL of B complex 100, 250 mg of Dex-­ Panthenol, 100 mg of B6, 100 mcg of B12, and 1 g of calcium chloride. The same benefit can be obtained in 4 weeks with transdermal 25% magnesium chloride lotion. ll Lithium orotate, 15 to 40 mg daily. This is particularly essential for those with bipolar depression but may expedite recovery in nearly all mood disorders. ll Vitamin D deficiency. 50,000 IU of D3 and 100 mcg of K2 may help nearly all these individuals. ll Adequate protein intake. In the most severe cases, supplements of taurine, 3000 mg, or tryptophan, 2000 to 4000 mg, may be helpful, with adequate B complex. ll Education: Although brief counseling intervention may be essential, education and self-therapy appear most effective. The book, 90 Days to Stress-Free Living by C. Norman Shealy provides a 3-month daily program which has shown to be effective in those willing to follow the treatment plan. ll Severe cases of PTSD need additional counseling, including techniques such as Gestalt therapy, psychosynthesis, guided imagery, EEG biofeedback, meditation, vibratory music, massage, and so on. ll Autogenic training: There is excellent evidence that daily practice of autogenic training over a period of 6 months leads to homeostasis of mood as well as autonomic homeostasis.20 ll Autogenic training consists of six primary phrases, repeated for approximately 20 minutes daily: ll My arms and legs are heavy and warm ll My heartbeat is calm and regular ll My breathing is calm and regular ll My abdomen is warm ll My forehead is cool ll My mind is quiet and still ll

Individual mind-body therapies may be useful for those with far less serious problems than PTSD. For example, in the author’s experience, for those with ADHD, lithium orotate and photostimulation may be adequate and lithium orotate at dosages of 45 mg per day is helpful in virtually all mood disorders, including PTSD.

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For migraines, temperature biofeedback is effective 84% of the time. These individuals also may respond well to stimulation with the Liss CES, or to avoidance of wheat, corn, eggs, milk, citrus, peanuts, and wine. They should always avoid aspartame. For rheumatoid arthritis patients, the entire protocol may be helpful. Additionally, stimulation with human DNA frequencies of 54 to 78 GHz applied with the SheLi TENS to 12 specific acupuncture points, called the Ring of Fire, has relieved the symptoms in 70% of RA patients who have failed conventional approaches. This approach has also been 80% effective in diabetic neuropathy.23 Epileptics are commonly deficient in magnesium and taurine and may respond to these supplements. Electroencephalogram (EEG) biofeedback training is also useful.24,25 Hypertension is often controlled with training in temperature biofeedback. Timed-release l-arginine and magnesium may also be of benefit.

Interface with Other Complementary and Alternative Modalities Ultimately, as Sir William Osler said more than 100 years ago, “More important than what the physician does, is the patient’s belief and the physician’s belief in what the physician does.” Benson, for instance, demonstrated that every 20th century treatment for angina pectoris, when subjected to double-blind controls was no better than placebo. The recent article “The Emperor’s New Drugs” has emphasized the remarkably minimal effect of antidepressants compared with placebo.26 Faith and belief appear to be key elements in all therapy. A positive attitude not only improves outcome but also positively affects quality of life. Even outcome of surgery is positively influenced by proper mental preparation. Ultimately, to a significant degree, the mind-body connection influences all therapy.

Research Summary and Conclusion There are well over 100,000 scientific articles emphasizing the effects of mind on body and of body on mind. The fields of hypnosis, biofeedback, relaxation training, psychoneuroimmunology, faith and prayer, and spirituality have solid scientific studies at this time. Some of the pertinent recent articles are listed subsequently.   1. Blizzard SJ, Kemppainen J, Taylor J. Posttraumatic stress disorder and community violence: An update for nurse practitioners. J Am Acad Nurse Pract. 2009;21(10):535-541.   2. Monson CM, Taft CT, Fredman SJ. Military-related PTSD and intimate relationships: From description to theory-driven research and intervention development. Clin Psychol Rev. 2009;29:707-714.   3. Feczer D, Bjorklund P. Forever changed: posttraumatic stress disorder in female military veterans, a case report. Perspect Psychiatr Care. 2009;45(4):278-291.   4. Gill JM, Saligan L, Woods S, Page G. PTSD is associated with an excess of inflammatory immune activities. Perspect Psychiatr Care. 2009;45(4):262-277.   5. Amstadter AB, Nugent NR, Koenen KC. Genetics of PTSD: Fear conditioning as a model for future research. Psychiatr Ann. 2009;39(6):358-367.   6. Lommen MJ, Restifo K. Trauma and posttraumatic stress disorder (PTSD) in patients with schizophrenia or schizoaffective disorder. Community Ment Health J. 2009;45:485-496.   7. Street AE, Vogt D, Dutra L. A new generation of women veterans: Stressors faced by women deployed to Iran and Afghanistan. Clin Psychol Rev. 2009;29:685-694.   8. Brand BL, Classen CC, McNary SW, Zaveri P. A review of dissociative disorders treatment studies. J Nerv Ment Dis. 2009;197(9):646-654.

  9. Vasterling JJ, Verfaellie M, Sullivan KD. Mild traumatic brain injury and posttraumatic stress disorder in returning veterans: Perspectives from cognitive neuroscience. Clin Psychol Rev. 2009;29:674-684. 10. Schnurr PP, Lumney CA, Bovin MJ, Marx BP. Posttraumatic stress disorder and quality of life: Extension of findings to veterans of the wars in Iraq and Afghanistan. Clin Psychol Rev. 2009;29:727-735. 11. Shin LM, Handwerger K. Is posttraumatic stress disorder a stressinduced fear circuitry disorder? J Trauma Stress. 2009;22:409-415. 12. Brewin CR, Lanius RA, Novac A, et al. Reformulating PTSD for DSM-V: Life after criterion A. J Trauma Stress. 2009;22:366-373. 13. Koenen KC, Amstadter AB, Nugent NR. Gene-environment interaction in post-traumatic stress disorder: An update. J Trauma Stress. 2009;22:416-426. 14. Peterlin BL, Katsnelson MJ, Calhoun AH. The associations between migraine, unipolar psychiatric comorbidities, and stress-related disorders and the role of estrogen. Curr Pain Headache Rep. 2009;13(5): 404-412. 15. Babson KA, Feldner MT. Temporal relations between sleep problems and both traumatic event exposure and PTSD: A critical review of the empirical literature. J Anxiety Disord. 2010;24:1-15. 16. Walsh DS. Interventions to reduce psychosocial disturbance following humanitarian relief efforts involving natural disasters: An integrative review. Int J Nurs Pract. 2009;15(4):231-240. 17. Asmundson GJ, Katz J. Understanding the co-occurrence of anxiety disorders and chronic pain: State-of-the-art. Depress Anxiety. 2009;26(10):888-901. 18. Litz BT, Stein N, Delaney E, et al. Moral injury and moral repair in war veterans: A preliminary model and intervention strategy. Clin Psychol Rev. 2009;29:695-706. 19. Sundin J, Fear NT, Iversen A, et al. PTSD after deployment to Iran: Conflicting rates, conflicting claims. Psychol Med. 2010;40:367-382.

Description of Landmark Studies/Books 1. Jacobson E. Progressive relaxation: A physiological and clinical investigation of muscular states and their significance in psychology and medical practice. University of Chicago Press; 1974, Original Copyright 1929. This study was done in 1929 and is considered by experts to be of Nobel Prize quality because it established the physiologic foundation of muscle and mental tension as major determinants of a majority of illnesses. The chapters on emotions, psychological factors, tone and nervous regulation, and the concept of neuromuscular hypertension make this an essential foundation for understanding the effects of muscle tension on the mind and the body.

2. Luthe W, Schultz JH. Autogenic Therapies. Vols 1-6. New York: Grune and Stratton; 1969. Volumes 1 and 4 are the most critical in this remarkable collection. There are some 2800 scientific articles with only 200 in English. Using a simple self-hypnotic technique, the authors demonstrated that 80% of what today is called “stress illnesses” could be well controlled with this approach.

3. Selye H. The physiology and pathology of exposure to stress: A treatise based on the concepts of the general adaptation syndrome and the diseases of adaptation. Montreal: ACTA, Medical; 1950. Again, this is one of the best scientific studies ever reported in a book and is considered by some experts to be of Nobel Prize quality. The book covers the physiology and pathology of stress on every known physiologic, hormonal, and metabolic system, as well as effects on various organs. The most critical aspect of Selye’s work is that he demonstrated that emotional and nervous stress produces the same biochemical physiologic responses as do chemical and physical stress.

4.  White L, Tursky B, Schwartz GE. Theory, Research and Mechanisms. New York: Guilford Press; 1985. This is the classic and best overall book on placebo and introduces the concept of “nocebo”. Essentially, every symptom and illness that can be triggered by disease, injury, or dysfunction can become a negative, conditioned response. These nocebo responses can elicit the same adversive reaction as the disease itself and the conditioned or learned response becomes a nocebo.

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228  Complementary and Alternative Medical Procedures 5. Pavlov IP. Conditioned Reflexes. Translated by Anrap GV. Oxford ­University Press; 1927. Again, the classic pavlovian conditioning work is extremely important in understanding totally unconscious reflex physiologic and psychological experiences, which can be initially imprinted by a single, strong physical, chemical, or emotional stress.

6. Benson H, Beary JF, Carol MP. The relaxation response. Psychiatry. 1974;37:37-46. This classic paper describes physiologic changes elicited by common mindbody practices such as meditation, yoga, autogenic training, and hypnosis. Evidence demonstrates that these learned techniques decrease oxygen consumption, respiratory and cardiac rate, and muscle tone, while increasing alpha rhythm brain activity and skin resistance. Opposite the ‘flight-orfight’ response of the sympathetic nervous system, the relaxation response, properly elicited in controlled conditions, has subsequently been shown to reduce postoperative anxiety and pain, decrease muscle tension in temporomandibular joint dysfunction, (TMJ) and other stress-related disorders, and positively affect many other disease states and health outcomes.

7. Goleman D, Gurin J. Mind-Body Medicine. Yonkers, New York: ­Consumer Reports Books; 1993. This is another book prepared for the public and has an excellent overview of the connections between mind, body, stress, emotions, and health.

8. Reich W. The Discovery of the Orgone. Translated by Wolfe TP. New York: Noonday Press; 1971. Reich’s concepts of body armoring and the physiologic and pathologic effects of muscle tension induced by mental distress is essential to understanding the remarkable breadth of possibilities in mind-body medicine.

9.  Tuke DH. Illustrations of the influence of the mind upon the body in health and disease. Elibron Classics. Adamant Media Corporation. Recognized as the first major book in the field of mind-body medicine, this classic is a most valuable resource.

10. Damasio A. Looking for Spinoza: Joy, Sorrow and The Feeling Brain. New York: Harcourt; 2003. A brilliant discussion of brain, body, and mind in the context of history, art, music, and philosophy.

Current Studies PubMed, the public-accessible version of the National Institutes of Health National Library of Medicine medical database, ­Medline, has 539 scientific references to mind-body medicine. When one considers many of the cross-references from this particular context, it is perhaps the best single source of scientific references. A PubMed search for psychoneuroimmunology yields at least 662 references, with many scientific potential cross-references.

Bibliography There are thousands of books and scientific articles that emphasize the mind-body connection. The following are suggested resources by mind-body medicine experts.

Books Benor DJ. Spiritual Healing: Scientific Validation of a Healing ­Revolution-Professional Supplement. Southfield, Mich. Vision. 2002. Davis J: Endorphins. Garden City, NY, Dial, 1984. Green E, Green A. Beyond Biofeedback. Ft. Wayne: In., Knoll; 1977. Ornstein R, Thompson RF. The Amazing Brain. Boston: Houghton Mifflin; 1984. Assagioli R. Psychosynthesis. New York: Penguin Books; 1965. Ballentine R. Radical Healing, Integrating the World’s Great ­Therapeutic Traditions to Create a New Transformed Medicine. New York: Harmony Books; 1997.

Benson H. The Relaxation Response. New York: Avon Books; 1975. Brown BB. New Mind, New Body: Biofeedback: New Directions for the Mind. New York: Harper Rowe; 1974. Coulter HL. Divided Legacy: A History of the Schism in Medical Thoughts. Vol. I- III. Washington, DC: Wehawken Book; 1975. Hanno K, Weisbrod J, Ericson K. Psychosocial and Behavioral Aspects of Medicine. Baltimore, Lippincott, Williams and Wilkins; 2003. Harris TA. I’m Okay-You’re Okay: A Practical Guide to Transactional Analysis. New York: Harper Rowe; 1969. Hastings AC, Fadiman J, Gordon J. Health for the Whole Person: The Complete Guide to Holistic Medicine. Boulder, Colorado: WestView Press; 1980. James W. The Varieties of Religious Experience: A Study in Human Nature. New York: Modern Library; 1936. Louis H, Martha E. Psychosomatics: How Your Emotions Can ­Damage Your Health. New York: Viking Press; 1972. Lynch J. The Language of the Heart. New York: Basic Books; 1985. Justice B. Who Gets Sick: Thinking and Health. Houston: Peak Press; 1987. McKeown T. The Role of Medicine: Dream, Mirage or Nemesis. ­London: The Nuffield Provincial Hospitals Trust; 1976. Norman SC. Life Beyond 100-Secrets of the Fountain of Youth. New York: Tarcher; 2006. Siegel BS. Love, Medicine, and Miracles. New York: Harper Rowe; 1986. Smuts JC. Holism and Evolution. New York: McMillan; 1926. Tart C. Open Mind, Discriminating Mind: Reflections on Human Possibilities. San Francisco: Harper Rowe; 1989.

Articles and Evidence-Based References Achterberg J, Lawliss GF, Simonton OC, Simonton S. Psychological factors and blood chemistries as disease outcome predictors for cancer patients. Multivariant Exp Clin Res. 1977;3:107-122. Angell M. Disease as a reflection of the psyche. N Engl J Med. 1985;312:1570-1572. Cunningham AJ. Mind, body, and immune response. In: Adey R, ed. Psychoneuroimmunology. New York: Academic Press; 1981, pp 609–617. Goldstein A, Grevert P. Placebo analgesia, endorphins, and naloxone. L ­ ancet. 1978;2:8104-8105. Ingelfinger FJ. Health: A matter of statistics or feeling. N Engl J Med. 1977;296:448-449. Wallace LM. Psychological preparation as a method of reducing the stress of surgery. J Human Stress. 1984;10:62-77.

Journals Advances: The Journal of Mind-Body Medicine Published by John E. Fetzer Institute Kalamazoo, MI 49009-9398 Subscription Department InnoVision Communications 169 Saxony Road, Suite 104 Encinitas, CA 92024 760-633-3910; 760-6333918 [email protected] http://www.fetzer.org/resources/resources_mindbody.htm American Journal of Health Promotion Michael P. O’Donnell, PhD, MBA, MPH, Editor Lawrence, Kansas

Mind Body Therapies and Posttraumatic Stress Disorder  229

800-783-9913 [email protected] http://www.healthpromotionjournal.com Journal of Behavioral Medicine W. Doyle Gentry, Editor-in-Chief [email protected] Kluwer Academic Publishers Order Department P.O. Box 358, Accord Station Hingham, MA 02018-0358 781-871-6600 866-269-WKAP 781-681-9045 (fax) [email protected] http://www.kluweronline.com/issn/0160-7715 Journal of Personality and Social Psychology Patricia G. Devine, Editor American Psychological Association Subscriptions 750 First Street, NE Washington, DC 20002-4242 202-336-5600 202-336-5568 [email protected] Journal of Psychosomatic Research Published by Elsevier Science http://www.elsevier.nl/inca/publications/store/5/2/5/4/7/4/ Pharmacopsychiatry B. Müller-Oerlinghausen, Berlin, Editor-in-Chief Thieme Publishers Stuttgart - New York [email protected]. http://www.thieme.de/pharmaco/ Psychosomatic Medicine [A journal published by the American Psychosomatic Medicine Society.] David S. Sheps, MD, MSPH, Editor-in-Chief http://www.psychosomaticmedicine.org/ Lippincott Williams & Wilkins PO Box 1600 Hagerstown, MD 21741 800-638-3030 301-223-2400 (fax) [email protected] Stress and Health Professor Graham D. Burrows, A.O., K.S.J., Editor-in-Chief Published by John Wiley and Sons. Ltd. New York, NY Subscription Inquiries John Wiley & Sons, Inc. Attn: Journals Admin Dept UK 111 River Street Hoboken, NJ 07030 201-7486645 [email protected] http://www.interscience.wiley.com/jpages/1532-3005 REFERENCES 1. Osler W. Aequanimitas: With Other Addresses to Medical Students, Nurses and Practitioners of Medicine. 2nd ed. Philadelphia: Blakiston’s; 1906. 2. Selye H. The Stress of Life. New York: McGraw-Hill; 1956.

3. Fact Sheet. Connecticut Clearinghouse. A Program of Wheeler Clinic. What is post-traumatic stress disorder? www.ctclearinghouse.org. Information provided by: New York State Office of Alcoholism and Substance Abuse Services 01/23/02. 4. Blanchard EB, Jones-Alexander J, BuckleyTC, et al. Psychometric properties of the PTSD checklist (PCL). Behav Res Ther. 1996;34(8):669-673. 5. Shalev AY, Peri T, Canetti L, Schreiber S. Predictors of PTSD in injured trauma survivors: A prospective study. Am J Psychiatry. 1996;153:219-225. 6. Foa EB, Riggs DS, Gershuny BS. Arousal, numbing and intrusion: Symptom structure of PTSD following assault. Am J Psychiatry. 1995;152:116-120. 7. Shin LM, McNally RJ, Kosslyn SM, et al. Regional cerebral blood flow during script-driven imagery in childhood sexual abuse-related PTSD: A PET investigation. Am J Psychiatry. 1999;156:575-584. 8. Liberzon I, Taylor SF, Amdur R, et al. Brain activation in PTSD in response to trauma-related stimuli. Biol Psychiatry. 1999;45(7):817-826. 9. Brady KT. Posttraumatic stress disorder and comorbidity: Recognizing the many faces of PTSD. J Clin Psychiatry. 1997;58(9):12-15. 10. Schnurr PP, Friedman MJ, Rosenberg SD. Premilitary MMPI scores as predictors of combat-related PTSD symptoms. Am J Psychiatry. 1993;150:479-483. 11. Andrews B, Brewin CR, Ross S, Kirk M. Predicting PTSD symptoms in victims of violent crime: The role of shame, anger, and childhood abuse. J Abnorm Psychol. 2000;109(1):69-73. 12. Shealy CN. The Pain Game. Millbrae, Calif: Celestial Arts; 1976. 13. Kilpatrick DG, Ruggiero KJ, Acierno R, et al. Violence and risk of PTSD, major depression, substance abuse/dependence, and comorbidity: Results from the National Survey of Adolescents. J Consult Clin Psychol. 2003;71(4):692-700. 14. Eysenck HJ. Personality, stress and cancer: Prediction and prophylaxis. Br J Med Psychol. 1988;61:57-75. 15. Shealy CN, Thomlinson P. Safe effective nondrug treatment of chronic depression: A review of research on low-voltage cranial electrical stimulation and other adjunctive therapies. Complementary Health Pract Rev. 2008;13:92-99. 16. Ader R. On the development of psychoneuroimmunology. Eur J Pharmacol. 2000;405:167-176. 17. Solomon GF, Moss RH. Emotions, immunity and disease: A speculative theoretical integration. Arch Gen Psychiatry. 1964;11:657-674. 18. Pert C. Molecules of Emotion: The Science Between Mind-Body Medicine. New York: Touchstone; 1999. 19. Shealy CN. Biogenic Health Maintenance. La Crosse, Wisc: Self Health Systems, 1976. 20. Schultz JH, Luthe W. Autogenic Training. Vols 1-6. New York: Grune & Stratton; 1969-1972. 21. Green E, Green A. Beyond Biofeedback. New York: Delacorte; 1977. 22. Shealy CN. Electromagnetic dysthymia. J Neuro Orthop Med Surg. 1997;17(3):193-195. 23. Shealy CN, Myss CM. The ring of fire and DHEA: A theory for energetic restoration of adrenal reserves. Subtle Energies. 1995;6(2):167-175. 24. Shealy CN, Burton S, Murrell M. Intracellular magnesium deficiency in chronic disease. Frontier Perspect. 2002;11(2):6-7. 25. Shealy CN. Electromagnetic dysthymia. J Neurol Orthop Med Surg. 1997;17(3):193-195. 26. Kirsch I, Moore TJ, Scoboria A, et al. The Emperor’s New Drugs: An analysis of antidepressant medication. Prevention and Treatment Jul 2002, 5(1):ArtID23.

22

Basic Principles of Neural Blockade

23

Jordan L. Newmark, MD

Since antiquity, man has searched for the ability to provide local and/ or regional anesthesia. Numerous methods have been described in historical texts, including the application of cold/ice, compression, rubbing, and acupuncture to painful areas. In the mid-1880s, cocaine was being studied in Peru. Soon after, it began to be used in medicine as a local and regional anesthetic in the United States and Europe for minor surgeries and dental procedures. Since that time, our understanding of macro and micro neuroanatomy, cellular biology, and pharmacology, has vastly expanded. This has allowed for entire medical subspecialties, such as regional anesthesia, pain medicine, and the like, to have developed and serve a vast array of patients. Local or regional anesthesia is indicated for a diversity of clinical circumstances (Table 23-1). It is easy to provide when one understands the regional anatomy, block technique, and pharmacology of the agents injected. These nerve blocks can provide anesthesia for procedures, as well as rapid diagnostic, prognostic, and therapeutic data when applied in the appropriate clinical setting. The result, either temporary or permanent, allows for pain relief, increased functionality, and independence, especially within the context of a well-designed, multidisciplinary pain treatment program. However, these positive outcomes may only occur when provided to the appropriate patient. The clinician must understand when providing a regional anesthetic may be contraindicated (Table 23-2).1 The American Society of Anesthesiologists (ASA) sets standards for the safe practice of anesthesia, including that for neural blockade.2 This includes appropriate monitoring of the patient and immediate access to supplemental oxygen and resuscitation equipment, in the rare occurrence of a catastrophic event. However, the ASA standards were written for perioperative patients, and not those presenting to the pain clinic. There is no official standard for monitoring within the realm of pain medicine. However, a recent survey of various pain centers within the United States demonstrated that for peripheral nerve blocks, 56% place a noninvasive blood pressure cuff and 52% place a pulse oximeter during the procedure.3 This is despite the fact that 72% of pain clinics had treated an average of 7.3 vasovagal reactions within the 12-month study period.3 Periprocedure nothing by mouth (NPO) status is another area in which the ASA has clear guidelines, yet these too are lacking for patients undergoing office-based neural blockade. The Joint Commission on the Accreditation of Healthcare Organizations (JCAHO) expects that universal protocols, such as preprocedure patient and site verification, as well as procedural time-outs, occur, before an anesthetic or invasive intervention is instituted. These standards also apply for neural blockade.3a

Neurovascular Bundle Anatomy The neurovascular bundle consists of peripheral nerve fibers wrapped in connective tissue, intermingled by a capillary plexus (Fig. 23-1). Three types of connective tissue are present within the peripheral nerve: endoneurium, perineurium, and epineurium. The endoneurium is a delicate, supporting structure located adjacent to individual axons within a fascicle. This layer covers the entire individual nerve fiber. Individual fascicles are bound by the perineurium.4,5 The perineurial barrier is formed by adjacent perineurial cells via tight junctions, which help manage the axonal microenvironment, in addition to the blood-nerve barrier and nerve-cerebrospinal fluid (CSF) barrier.6 The fascicles are bound in groups by the outermost layer, the epineurium (Fig. 23-2), which encloses the nerve as a whole. This layer contains the vasa nervorum, which divides into arterioles that penetrate the perineurium (Fig. 23-3). Ultimately, a network of capillaries reaches each fascicle to supply individual axons. More specifically, the vasa nervorum forms the endoneurial capillaries. The endoneurial capillary endothelium contains tight junctional connections, which create the blood-nerve barrier. Cells that compose the distal layer of the arachnoid membrane are connected by tight junctions as well, which form the boundary of the nerve-CSF barrier. As nerve roots leave the subarachnoid space, the perineurium fuses with the cells of the distal layer of the arachnoid membrane. Anterior and posterior nerve roots, which are motor and sensory, respectively, initially leave the spinal cord separately, but merge via the connective tissue architecture, to become mixed sensorimotor nerves exiting the spinal canal.6 The neurovascular bundle usually lies well protected between muscle or bone. At its most proximal location—the spinal root level—the neurovascular bundle contains motor, sensory, and autonomic fibers. These roots divide into dorsal and ventral rami, the latter of which reconnect to form a plexus of nerves. Ultimately, terminal nerve branches of isolated fiber types—sensory or motor branches—are formed.

Local Anesthetic Pharmacology Local anesthetic agents are categorized by their chemical composition—esters and amides (Table 23-3). Ester and amide anesthetics are weak bases—their pKa is near physiologic pH. Each is comprised of a lipophilic group, such as a benzene ring, and a hydrophilic group, such as a tertiary amine. These groups are either 233

234  Peripheral Nerve Blocks

Table 23-1  Indications for Percutaneous Nerve Blocks With Local Anesthetics Provides anesthesia for procedures Differentiates pain problems and helps better understand nociceptive pathways

Table 23-2  Relative and Absolute Contraindications for Regional Anesthesia1 Patient Selection Factors

Relative Contraindication

Absolute Contraindication

Patient  cooperation

Psychiatric disorder  (e.g., needle phobia, anxiety)

Patient refusal

Serves as a treatment for inflammatory compression neuropathies in combination with corticosteroids

Movement disorder  (e.g., essential tremor, tics)

Provides treatment for sympathetic mediated pain syndromes Differentiates spasticity from joint contractures

Language barrier,  pediatric patient

Helps predict the effect of a neurolytic procedure Allows selective recording in nerve conduction studies7 Promotes functional activities in an occupational or physical therapy program Assists in serial or inhibitory casting With Normal Saline Provides placebo response With Neurolytic Agents (Chemical Neurolysis)

Acutely intoxicated Anatomic and physiologic

Anatomic abnormalities

factors

Technical challenges (e.g., obesity, arthritis)

Anesthetic  considerations

Lack of clinician knowledge, skill, or ability (e.g., nerve stimulation) Lack of equipment for block placement, monitoring and resuscitation (e.g., oxygen delivery)

Facilitates functional goals in the spastic patient: positioning,  ambulation, bracing, transfers Improves caregiver tasks (such as hygiene) in the spastic patient:  perineal, axillary, elbow, or hand regions Improves self-image of the spastic patient by reducing joint  deformities and improving cosmesis

Coexisting diseases

May improve residual voluntary muscle control by eliminating unwanted hypertonia in the spastic patient

Neurological disease (e.g., multiple sclerosis)

Infection at injection site

Comatose state

Allergy to anesthetic

Sepsis

Coagulopathy/systemic anticoagulation

Reduces pain caused by hypertonia Provides treatment for specific, intractable pain disorders

Coagulopathy  (e.g., hemophilia)

Prevents nerve compression injuries in hyperflexed joints (i.e., median nerve at the wrist from wrist flexor spasticity)

Trauma (especially neurological trauma)

Prevents skin breakdown by promoting proper seating and positioning Perioperative issues

connected by an ester or amide linkage. This linkage is what imparts their categorization as an ester or amide. Esters are readily metabolized by plasma cholinesterase, thus their half-life is very short, on the order of minutes. Para-aminobenzoic acid (PABA) is one of the break-down products of this reaction. Amides undergo hepatic metabolism through N-dealkylation and hydrolysis. This is a slower process, imparting a longer half-life (2 to 3 hours), assuming the patient has normal liver function. Some patients with local anesthetic allergy may be sensitive to PABA, and a detailed history and chart review may be necessary to delineate if a ester local anesthetic was really the causative agent responsible for an earlier allergic reaction. Some local anesthetics, esters and amides alike, are stored in multi-use vials with the preservative methylparaben. Methylparaben may also cause an allergic reaction in patients with a PABA allergy.8 All local anesthetics are weak bases, and their pKa is near physiologic pH. This allows for these agents to be present in both the ionized (charged) and nonionized (uncharged) forms when administered. The lower the agent’s pKa and higher the pH, the more that will be uncharged in-vivo. The uncharged local anesthetics are lipophilic and readily cross cell membranes, namely neuronal axons. Thus, the more uncharged local anesthetic that exists in vivo for a given agent, the more potent and

Surgical duration to outlast regional anesthetic

Block will hinder the procedure

Surgical positioning discomfort Prolonged surgical time Adapted from Tsui, BCH, Finucane, BT: Managing adverse outcomes during regional anesthesia. In Longnecker DE, Brown DL, Newman MF, Zapol WM (eds):  Anesthesiology. New York, McGraw Hill, 2008, p 1054.

faster onset that agent is rendered. For this reason, clinicians will elect to add sodium bicarbonate to their local anesthetics, to raise the pH and thereby increase the amount of nonionic local anesthetic. Local anesthetics act on neuronal axons. These agents, when uncharged, passively diffuse to the sodium channels of axons. These sodium channels allow Na+ to enter the axon, depolarize, and propagate an action potential to allow for communication between neurons. Local anesthetics inhibit this process by binding to these sodium channels, ceasing depolarization as well as action potential propagation, and thus neuronal signaling and transmission of pain signals (Tables 23-4 and 23-5). Local anesthetics block in a sequential order, which is related to the diameter of the axon (see Tables 23-4 and Table 23-5). C-fibers,

Basic Principles of Neural Blockade  235

23

F F

F

EV

Figure 23-1  Under magnification, the neurovascular bundle with extrinsic blood vessels and a segmental supplying artery are apparent (EV). The linear extrinsic vessels parallel grooves created by adjacent fascicles (F). (From Beek AV, Kleinert HE: Peripheral nerve injuries and repair. In Rand R [ed]: Microneurosurgery, 3rd ed. St. Louis, Mosby, 1985, p 742, with permission.)

Figure 23-3  Neurovascular bundle demonstrating the entrance of the arterial supply into the epineurium with surrounding connective tissue. (From Zancolli EA, Cozzi EP: Nerves of the upper limb. In Zancolli EA, Cozzi EP [eds]: Atlas of Surgical Anatomy of the Hand. New York, Churchill Livingstone, 1992, p 685, with permission.)

Table 23-3  Categorization of Local Anesthetic Agents GROUP

Esters

Amides

Procaine

Lidocaine

Cocaine

Mepivacaine

Chloroprocaine

Bupivacaine

Tetracaine

Etidocaine Ropivacaine

FASC

Figure 23-2  Under magnification, a cross-section of the median nerve demonstrates individual and groups of fascicles (FASC). Note the connective tissue between each fascicle and surrounding the entire nerve. (From Beek AV, Kleinert HE: Peripheral nerve injuries and repair. In Rand R [ed]: Microneurosurgery, 3rd ed. St. Louis, Mosby, 1985, p 742, with permission.)

which carry pain and temperature information, are blocked first, as their diameter is small. A-α and A-β fibers have the largest axonal diameter, and are the last to become blocked. These fibers are primarily motor and proprioceptive. However, nerves with myelin may only require pharmacologic sodium channel blockade at the nodes of Ranvier, leaving these nerves susceptible to local anesthetic action.8

Mechanical or chemical vasoconstriction is sometimes beneficial for local anesthesia. It allows for a block of longer duration and stronger intensity by decreasing systemic uptake. This also imparts protection against systemic local anesthetic toxicity. Dilute epinephrine is the most common agent added to local anesthetics for this purpose, although phenylephrine and norepinephrine may also suffice, with lesser results.9 Epinephrine dilutions of 1:200,000 (5 mcg/mL) and 1:400,000 (2.5 mcg/mL) are typically prepared with the local anesthetic. An added benefit of adding epinephrine is that it may serve as an early indicator of unintentional vascular injection. This is sometimes referred to as a “test dose”, whereby a small dose of local anesthetic with epinephrine is injected while the patient’s heart rate is monitored. An increase in heart rate above 20% of the baseline heart rate would confer a positive test dose, indicating an intravascular injection may have occurred. There are potential contraindications to the addition of a chemical vasoconstrictor to local anesthetics, although the evidence for these may be weak10 (Table 23-6). Furthermore, chemical tourniquets should not be used when anesthetizing digits, ears,

236  Peripheral Nerve Blocks

Table 23-4  Classification of Nerve Fibers8,11 Letter Class

Numeral Class

Diameter (μm)

Conduction (msec)

Myelin

Drug ­ ensitivity S

Function

—

Ia

12-20

70-120

++

++

Muscle spindle primary endings

—

Ib

12-20

70-120

++

++

Golgi tendon organs

A-α

—

6-22

70-120

++

++

Motor efferent, proprioception afferent

A-β

II

6-22

30-70

++

++

Motor efferent, proprioception afferent, encapsulated an  accessory structured nerve endings (e.g., Meissner  corpuscles) Muscle spindle efferent

A-γ

—

3-6

10-50

++

++

A-δ

III

1-4

5-30

++

+++

B

—

<3

3-15

+

++++

Preganglionic autonomic

C

IV

0.3-1.3

0.5-2

—

++++

Pain, temperature (warm), afferent, itch, postganglionic  autonomic

Pain, temperature (cold), touch, afferent, hair receptors

Adapted from Jin P, Min C: Local anesthetics. In Dunn PF, Alston TA, Baker KH, et al (eds): Clinical Anesthesia Procedures of the Massachusetts General Hospital. Philadelphia, Lippincott Williams & Wilkins, 2007, p 239; and from Nolte J: Sensory receptors and the peripheral nervous system. In Nolte J: The Human Brain: An Introduction to Its Functional Anatomy. St. Louis, Mosby, 2002, pp 219-220.

Table 23-5  Relative Size of Peripheral Nervous System Axons and Associated Functionality11

Class

Relative Axonal Diameter

Afferent Function

Ia

++++

Muscle spindle

Ib

++++

Golgi tendon  organ

A-α

++++

A-β

+++

A-γ

+++

A-δ

++

Sharp pain, cold, some touch

Preganglionic  autonomic

C

+ (No Myelin)

Dull pain, heat, itch

Postganglionic  autonomic

Efferent Function

Lower motor neuron Meissner and pacinian corpuscles, Merkel endings Axons to intrafusal fibers

Adapted from Nolte J: Sensory receptors and the peripheral nervous system. In Nolte J: The Human Brain: An Introduction to Its Functional Anatomy. St. Louis, Mosby, 2002, pp 219-220.

Table 23-6  Relative Contradictions to the Addition of Chemical Vasoconstrictors to Local Anesthetics Hypertension (essential or secondary) Cardiovascular disease (e.g., coronary artery disease, arrhythmias, etc…) Hyperthyroidism Uteroplacental insufficiency8 Pheochromocytoma Drug-drug interactions: Tricyclic antidepressants Monoamine oxidase inhibitors Nonselective β-blockers

Table 23-7  Grade C Evidence for Adjusting the Maximum Allowable Dose of Local Anesthetics Maximum allowable dose may be increased: Use of chemical or mechanical vasoconstriction or tourniquets Administration within the urinary bladder, intact skin, ischemic tissue Maximum allowable dose may be decreased: Newborns (<4 months of age) age >70 years Decreased renal function or uremia Hepatic dysfunction Advanced heart failure or shock Pregnancy Inhibitors of CYP liver enzymes of the P450 system (e.g., itraconazole fluvoxamine) Adapted from Rosenberg PH, Veering BT, Urmey WF: Maximum recommended doses of local anesthetics: A multifactorial concept. Reg Anesth Pain Med. 29(6):564-575, 2004.

noses, genitals, or other areas with a poor collateral blood supply because this could lead to tissue necrosis. However, several recent large trials and literature reviews failed to demonstrate consistent tissue injury from the use of chemical vasoconstriction in some of these areas.12-14 What is the maximum allowable dose of local anesthetic that can be administered to the patient? This is a common question asked of clinicians, and it can be a source of confusion. The answer varies, and can depend on factors such as the local anesthetic used, to even the country in which the clinician is practicing. First, it is recommended that the package insert for the local anesthetics used be reviewed as a basis for dosing guidelines. However, a recent review of the maximum allowable dose of common local anesthetics found grade C evidence for dose adjustments depending on several factors (Table 23-7).15 Within the United States, 300 mg of lidocaine is considered the maximum allowable dose. Interestingly, the source for this cannot be found in the scientific literature.15

Basic Principles of Neural Blockade  237

23

Neural Block Technique: General Considerations Peripheral nerve blockade can be obtained through a variety of techniques. However, to accomplish a successful block, the clinician must have a detailed understanding of the relevant anatomy, as well as technical skill. When selective motor nerves are blocked, knowledge of kinesiology is useful. To safely block a nerve of choice, local anesthetic must be deposited into the nerve sheath, or epineural space, and not intraneurally. The following techniques will describe the basic principles of approaching the nerve, such that local anesthetic can be safely given, without resulting in an intraneural injection. In preparation for these procedures, neural blocks should always be performed under sterile conditions. An antiseptic skin preparation, sterile equipment, sterile gloves, as well as masks and caps being worn are essential elements in reducing the risk of inoculating the patient with an infectious agent. A short-acting premedication may be given to the patient to reduce anxiety and pain, such as midazolam or fentanyl. However, the clinician must not give so much sedation that communication breaks down, and paresthesias cannot be appreciated during the block procedure. Needles used for neural blockade are often stiff; to allow for deep penetration, 23- and 22-gauge needles ranging from 25 to  150 mm in length are commonly used, depending on the type of block and procedure to be carried out. Needle trauma (discussed subsequently) is always a concern during neural blockade, and several needle bevel types are available. Sprotte and Whitacre tips, as well as short-bevel needles, are associated with less nerve trauma when compared with standard A-bevel needles.16 The two common approaches used to block nerves are the paresthesia technique (PT) and nonparesthesia technique (NPT), also known as a field block. PT attempts to purposefully provoke paresthesias of the nerve before injection. These paresthesias indicate that the needle is in contact with the nerve and serve as a warning of potential nerve injury. This technique assumes that the patient’s sensory pathways are intact and that the patient is able to cooperate with the procedure. However, this method can be uncomfortable, and can potentially damage the nerve of interest.17-19 To help avoid neural injury, the clinician should make every effort to stop, reposition, and refrain from injecting whenever a serious or persistent paresthesia occurs. The second approach, NPT, avoids this deliberate probing for paresthesias and relies on anatomic landmarks, but generally requires greater volumes of local anesthetic. NPT is best suited for superficial nerves, and often helps supplement a prior regional anesthetic which may be inadequate over certain areas. NPT uses dilute, high volumes of local anesthetic, with the addition of epinephrine, to reduce the risk of local anesthetic toxicity.20 With NPT, the needle tip may not approximate the nerve as closely as with PT. However, to provide the safest regional anesthetic, PT should be avoided when possible. Electrical stimulation (Fig. 23-4) can be used to locate and block peripheral nerves. These stimulators are available commercially, although office electrodiagnostic equipment often will suffice. An electrical impulse generated by the stimulator and controlled by a rheostat is transmitted through the needle. A ground electrode is placed on the patient and connected to the positive lead, while the negative lead is connected to the needle. Insulated needles are available, many of which are covered with materials such as polytetrafluoroethylene (Teflon). In general, insulated

Figure 23-4  As the physician holds the syringe in his right hand, the rheostat is adjusted on the block stimulator with the left hand. The syringe is attached to a Teflon-coated hypodermic needle, which is attached to the stimulator. Note the surface ground pad on the patient’s inner thigh.

needles are preferred over noninsulated needles. As the needle approaches the nerve, either a motor, sensory, or mixed response can be elicited, depending on the fiber types contained within the nerve. Typically, the clinician looks for a twitch in the expected muscle group associated with the nerve. This twitching is not typically uncomfortable for the patient; however, if it is painful in anyway, the needle should be redirected. The neural response should increase as the needle tip approaches the nerve. It is desirable to obtain a strong neural response with a low stimulus output, thereby ensuring needle placement is sufficiently distant from the nerve to provide anesthesia, yet prevent an intraneural injection. This technique is preferred when injecting neurolytic agents for the treatment of spasticity. One can quickly identify selective motor responses and quickly determine the effect of chemical neurolysis after injection. The use of ultrasound guidance for peripheral nerve blockade has become popular in recent years, allowing the clinician to incorporate real-time, two-dimensional, visual data, in conjunction with electrical nerve stimulation data, to facilitate block procedures. Continuous neural blockade can be achieved through the use of perineural infusion indwelling catheters (Fig. 23-5). These catheters are most commonly placed perioperatively for postoperative pain from ambulatory orthopedic surgery. These catheters can be used in the hospital or at home by the patient in recovery for several days by way of infusion pumps. There are even case reports of portable pumps, which allow the patient to ambulate and regain independence.21 Both continuous infusions, as well as patient-controlled regional anesthesia systems have been described.22 These catheters must be placed under strict sterile conditions because these are indwelling devices that remain in the patient for days. Potential complications include nerve injury and transient neurologic damage, infection, associated unwanted nerve blockade, and local anesthetic side effects and toxicity.22 Computed tomography (CT) guidance for peripheral nerve blockade has also been described as an effective means to provide regional anesthesia, especially in patients where the relevant anatomy is difficult to identify (Fig. 23-6).23 This form of image guidance for neural blockade allows for excellent visualization of the

238  Peripheral Nerve Blocks

anatomy and appropriate spread of local anesthetic. CT-guided nerve blocks are not commonly used because they require expensive equipment and trained radiology technicians. Radiation exposure to the patient and care providers is a concern in performing CT-guided blocks. Regardless of the technique, the needle tip should always remain in the epineural space during an injection (Fig. 23-7). Intraneural injections have a high association with fascicular damage.24,25 If paresthesias are elicited, the needle should be repositioned before

local anesthetic solution is injected. Forceful injection is never recommended because it may be a sign of injecting into a fixed space, such as tendon or adjacent to bone. Repeat anesthetic injections close to the same nerve in a single patient encounter should be avoided because warning paresthesias may be suppressed and occult iatrogenic nerve injury may occur. Accidental intravascular injection of local anesthetic is an unintentional event with potentially life-threatening results. To avoid this, slow administration of local anesthetic is advisable to allow detection of early side effects, such as tinnitus, perioral numbness, or tachycardia. Intravascular injection can usually be avoided by frequently aspirating for blood in several planes prior to, and during, a slow injection, by pulling back on the syringe plunger. Most importantly, an understanding of the relevant anatomy, clinician diligence, as well as a plan to treat and resuscitate the patient from an inadvertent intravascular injection, will maximize the chance for a positive patient outcome.

Nerve Injuries

Figure 23-5  Longitudinal approach to the continuous interscalene block. A 17- to 18-gauge insulated Touhy needle is placed on the superior root of the brachial plexus with the aid of a nerve stimulator. Once placed, the nerve stimulator is attached to the proximal end of a 19- to 20-gauge stimulating catheter, which conducts electricity to the tip of the catheter. The catheter is advanced 3 to 5 cm beyond the needle tip, while maintaining an unchanged motor response. (From Boezaart AP: Perineural infusion of local anesthetics. Anesthesiology 104(4):872-880, 2006.)

Trauma, toxicity, and ischemia are the major causes of nerve injury during neural blockade. Nerve injection injuries are almost always due to one or more of these factors.18 The incidence of neural injury during block procedures is about 1% to 2%, most of which are minor in nature.26 Trauma to the nerve during neural blockade occurs with aggressive probing during needle insertion. This can directly injure the nerve fascicles. Additives, such as epinephrine, increase the toxicity of the anesthetics when injected intrafascicularly.26a,27,28 Selander and colleagues showed a reduction in the incidence of nerve trauma and fascicle injury when short, beveled needles were used. They also demonstrated that nerve fascicles rolled or slid with needle contact.18 Most traumatic nerve injury symptoms selfresolve in 4 to 6 weeks, and essentially all reach resolution within 12 months.27 Intraneural injections of solution not only directly injure nerve fibers, but also cause damage to the blood-nerve barrier function.24,25 The spread of anesthesia with intraneural injections has been demonstrated and, when near the spine, may cause unexpected spinal anesthesia.29 Neural compression or stretching also

J C

A

A

M

M V

A

B

Figure 23-6  Brachial plexus block to treat a left C7 mononeuropathy. A, Transverse contrast-enhanced CT scan, obtained after the skin over the brachial plexus was marked with barium paste (arrows), was acquired to help identify the locations of the common carotid artery (C), internal jugular vein (J), and vertebral artery (V). A, anterior scalene muscle, M, middle scalene muscle. B, Transverse CT scan demonstrates the tip of the needle inserted within the plane separating the anterior and middle scalene muscles. (From Mukherji SK, Wagle A, Armao DM, Dogra S: Brachial plexus nerve block with CT guidance for regional pain management: initial results. Radiology 216:886-890, 2000.)

Basic Principles of Neural Blockade  239

may result from large volumes of solution injected into a fixed space, thereby traumatizing the nerve. Neurotoxicity can be caused by direct injection of anesthetics into nervous tissue—intrafascicular injections can cause profound or permanent nerve damage. The degree of damage depends on the type and amount of drug injected, as well as the kind of preservative used for the anesthetic medication.24,25 Ester anesthetics generally demonstrate greater toxicity than amides when injected into the intrafascicular space.30,31 Extrafascicular injections of anesthetics in routine concentrations rarely cause significant histologic nerve damage or disruption of the blood-nerve barrier, but can alter the permeability of the perineurium, leading to endoneurial edema.30,31 The epineurium provides some neuroprotective function during injection, thereby reducing toxicity from anesthetic medication. Mackinnon and colleagues found that corticosteroid injections into the epineural tissue did not cause nerve damage.32 When injected into the intrafascicular space, corticosteroids exerted a B A

Figure 23-7  Needle placement in the intrafascicular space (A) compared to the extrafascicular space (B). (Adapted from Gentili F, Hudson A, Kline D, et al: Peripheral nerve injection injury: An experimental injury. Neurosurgery 4:244-253, 1979, © Congress of Neurological Surgeons.)

A

B

direct neurotoxic effect with disruption of the blood-nerve barrier, similar to anesthetics. Severe nerve fiber damage was noted with hydrocortisone (Solu-Cortef ) and triamcinolone hexacetonide (Aristospan), moderate damage with triamcinolone acetonide (Kenalog) and methylprednisolone (Depo-Medrol), and the least damage with dexamethasone (Decadron) (Fig. 23-8). Ischemia is typically thought to be the result of the application of a tourniquet for a prolonged time period, or improper positioning of the patient. However, a nerve block itself, if the injection is given into the intrafascicular space, may also cause ischemic damage. The ischemia results from increased intraneural compartment pressure by the injectate volume, which reduces neural perfusion. This intraneural pressure has been shown experimentally to remain above the blood perfusion pressure for 15 minutes without damage.29 A rare potential cause of ischemic nerve injury is the result of a local hematoma formed during the block procedure from inadvertent arterial puncture. To diagnose a neural injury, a combination of radiologic imaging and electrophysiologic tests can be performed in conjunction with the patient’s history and physical examination. Obtaining input from other specialty consultants, such as neurologists and radiologists, often hastens appropriate testing and diagnosis of a potential nerve injury. Magnetic resonance imaging (MRI) can be useful in revealing nerve compressions secondary to fluid accumulation from blood, edema, or local anesthetic injectate.26 Conduction tests can be used to assess the amount of damage to large diameter sensory and motor axons. Electromyography (EMG) can evaluate and quantify damage to smaller motor units26 as well as help with locating the site of neuronal injury. Patients with an underlying peripheral neuropathy, either known or subclinical, may be more susceptible to nerve injury during neural blockade, a phenomenon known as the “double crush” syndrome (Fig. 23-9). The double crush syndrome hypothesis claims that damaged axons may be more prone to damage at a more distal location.33 Furthermore, two relatively small lesions along a single axon are worse than a single larger lesion—the damage of two axonal stressors “far exceeds the expected additive damage

C

Figure 23-8  A, Cross-section of a normal myelinated nerve fiber population within a sciatic nerve (×585). B, Cross-section 12 days after intrafascicular injection of dexamethasone (Decadron), demonstrating relatively normal appearance with minimal evidence of nerve injury (×585). C, Cross-section 12 days after intrafascicular injection of triamcinolone hexacetonide (Aristospan), demonstrating severe widespread axonal and myelin degeneration (×585). (From Mackinnon SE, Hudson AR, Gentili F, et al: Peripheral nerve injection injury with steroid agents. Plast Reconstr Surg 69:482-489, 1982, with permission.)

23

240  Peripheral Nerve Blocks Cell body Axoplasmic flow

Axon

(A)

(B) X

(C) X1

X2

X

(E) X

caused by each isolated compression”.33 For example, a case report in 2001 of a young female undergoing chemotherapy with cisplatin, an agent known to cause peripheral neuropathies, developed a brachial plexopathy after an interscalene block.33 Bearing this in mind, patients with a potential initial axonal insult from any cause, may be susceptible to nerve damage from subsequent neural blockade.

General Principles of Neural Blockade A number of agents, and combinations, are often used to provide a nerve block. The most common mixtures include local anesthetics with corticosteroids. When chemical neurolysis is desired, such as with hypertonicity or chronic intractable pain, neurolytic drugs (e.g., phenol), may be administered. A brief discussion of the principles of anesthetic, motor, sensory, and neurolytic blocks follows.

Anesthetic Blocks Because local anesthetics are reversible, nerve blocks can be performed to intentionally paralyze or deactivate specific muscles and/or selectively disrupt sensory pathways. This effect has numerous clinical applications, especially when prior treatment has failed or a diagnosis is unclear. With the exception of anesthesia for surgical procedures, anesthetic blocks should seldom be the initial treatment of a disorder but may be integrated into a comprehensive rehabilitation program.

Motor Blocks Isolated blocks purely to motor nerves, or to motor components of mixed nerves, are useful to relax specific muscles. Motor blocks also may be useful in differentiating joint contracture from

Denervation

(D)

Figure 23-9  Neural lesions resulting in denervation. Axoplasmic flow is indicated by the density of shading. Complete loss of axoplasmic flow results in denervation (C, D, E). A, Normal neuron. B, Mild neuronal injury at a single site (X) is insufficient to cause denervation. C, Mild neuronal injury at two separate sites (X1 and X2) may cause distal denervation. D, Severe neuronal injury at a single site (X) may also cause distal denervation. E, Diffuse underlying disease process (toxic, metabolic, ischemic) impairs axonal flow throughout the neuron that predisposes the axon to distal denervation after a single minor neural insult at X. (From Hebl JR, Horlocker TT, Pritchard DJ: Diffuse brachial plexopathy after interscalene blockade in a patient receiving cisplatin chemotherapy: The pharmacologic double crush syndrome. Anesth Analg 92:249-251, 2001.)

spasticity. For example, if a patient presents with an elbow flexion deformity, a musculocutaneous anesthetic nerve block can be performed. After injection, the patient’s elbow is passively extended, and any change in range of motion is evaluated. If only minimal improvement in passive elbow extension occurs, one would suspect contracture formation or bony ankylosis as the cause. However, if full extension is achieved, the elbow flexion deformity is more likely to be related to spasticity. A neurolytic block may then be pursued. The information gained from the previous anesthetic block assists the clinician in predicting the outcome from subsequent therapeutic neurolysis. In addition, anesthetic peripheral nerve blocks can facilitate serial casting by relaxing spastic muscles. The effect allows placement of casts on extremity joints in the desired position.

Sensory Blocks Anesthetic peripheral nerve blocks are most commonly used to facilitate surgical procedures by blocking sensory pathways. In an office practice setting, anesthetic blocks can be used to assist in the diagnosis of difficult pain problems.33a When sensory components to nerves are interrupted, expected dermatomal sensory changes can be evaluated and compared with actual blocked changes, thereby diagnosing nociceptive pain pathways previously unappreciated or undiagnosed. For example, a radial sensory neuropathy masked by de Quervain tenosynovitis may be diagnosed after a radial sensory nerve block.33b Other compressive neuropathies, such as carpal tunnel syndrome, may later require corticosteroid injections. Patients who are malingering, or who magnify symptoms, also may be evaluated using blocks. Response to injections with various concentrations of anesthetic versus placebo can be analyzed to evaluate the psychological component of the pain disorder.

Basic Principles of Neural Blockade  241

Another way to use sensory blocks is to “reset” the pain generators, especially in cases of sympathetic mediated pain disorders with serial injections.34 When a response to painful stimuli is attenuated, the patient can participate in a therapy program that emphasizes functional tasks, joint range of motion, stretching, and skin desensitization. The goal is to gradually eliminate the painful stimulus over time.

Neurolytic Blocks Spasticity Hypertonicity due to upper motor neuron dysfunction may be caused by lesions at many levels within the brain and spinal cord. Among patients with traumatic brain injury (TBI), the most severe hypertonicity is found in those with diffuse axonal injury (DAI) or hypoxic-ischemic injury (HII) following cardiopulmonary arrest. Rigidity, spasticity, and dystonia all contribute to joint abnormalities and restricted function. Hypertonicity is usually greatest within the first 6 months of injury. Because this is the period of spontaneous neurologic recovery, one should avoid any permanent surgical procedure intended to control hypertonicity. Without any treatment, disabling musculotendinous contracture and abnormal, dyssynergic patterns of movement occur, further complicating the patient’s recovery and outcome. Peripheral nerve blockade may be useful during this interval to aid in the treatment of spasticity. A large number of patients with TBI and spinal cord injury require localized nerve blocks designed to depress the final common pathway during reorganization and recovery of the central nervous system. Noninvasive treatment of spasticity should be maximized before proceeding with neurolytic blocks. This includes medications, stretching, serial casting, icing, electrical stimulation, and positioning. Any cerebral or spinal cord anomalies, such as hydrocephalus and syringomyelia, should be corrected surgically. Any noxious stimuli, such as urinary tract infection and skin lesion, should be eliminated when possible. Drug-induced movement disorders should be evaluated and, when possible, the offending drug should be discontinued. The prognosis for motor return and stage of recovery should be established. The physician must determine if the hypertonicity is generalized or focal. Generalized hypertonicity is usually not responsive to nerve blocks unless it is for the purposes of hygiene. Consistent patterns of hypertonicity need to be established and treatment should initially be directed toward proximal tone. Any block should affect the most proximal nerve capable of denervating the maximum number of spastic myotomes. All residual voluntary motor function of the affected limb is to be preserved. Phenol, a common neurolytic agent, generally results in alleviation of spasticity with little decrease of voluntary contraction.35 Pain Management The most common use of neurolytic agents for pain management is to treat intractable cancer pain in patients with a limited life span. This can be done with intrathecal or peripheral nerve injections. Advancements in radiofrequency procedures are rapidly replacing injectable neurolytics for pain management.

Education, Training, and Simulation Teaching clinical fellows, residents and medical students not only the informational and academic aspects of neural blockade, but also the technical procedures and associated ergonomics is important.

However, it is not always possible to expose trainees to enough procedures to allow them to perform these blocks individually in a safe and efficient fashion. High-fidelity simulators have become increasingly popular for trainees to gain these valuable skills. Likewise, simulation can allow trainees, and the practicing clinician alike, to manage rare complications and crisis situations as they relate to neural blockade (e.g., anaphylaxis). A recent case report describes how the use of simulation facilitated the management of a patient in cardiac arrest from bupivacaine toxicity.36 High-fidelity simulation for educating trainees to perform a variety procedures and managing critical events will likely become an essential component of medical education.

Conclusion Clinicians and patients alike have long shared the desire to achieve a safe and effective means to anesthetize regions of the body stricken by pain. The available techniques for neural blockade require the clinician to be familiar with, and understand, regional anatomy, indications, side effects, and local anesthetic pharmacology. With this knowledge and mastery of the technical aspects of these procedures, the patient can expect relief from the application of neural blockade. ACKNOWLEDGMENT The author would like to extend a special thank you to Ted Lennard, MD, for his original work on this chapter.

REFERENCES   1. Tsui BCH, Finucane BT. Managing Adverse Outcomes during Regional Anesthesia. In: Longnecker DE, Brown D, Newman M, Zapol W, eds. Anesthesiology. New York: McGraw Hill; 2008:1054.   2. American Society of Anesthesiologists. Standards for Basic Anesthetic Monitoring, 2005. http://www.asahq.org/For-Healthcare-Professionals/  ~/media/For%2520Members/documents/Standards%2520Guidelines  %2520Stmts/Basic%2520Anesthetic%2520Monitoring%25202005.ashx   3. Ahmed SU, Tonidandel W, Trella J, et al. Peri-procedural protocols for interventional pain management techniques: a survey of US pain centers.  Pain Physician. 2005;8:181-185. 3a. Kirvela O, Nieminen S. Treatment of painful neuromas with neurolytic blockade. Pain. 1990;41:161-165.   4. Ross MH, Reith EJ. Perineurium: Evidence for contractile elements. Science. 1969;165:604-606.   5. Thomas PK, Olsson Y. Microscopic anatomy and function of connective tissue components of peripheral nerve. In: Dyck PJ, Thomas PK, Lambert EH, Bunge R, eds. Peripheral Neuropathy. vol. 1. Philadelphia: WB Saunders; 1984:97-120.   6. Anthony DC, Frosch MP, Girolami UD. Peripheral nerve and skeletal muscle. In: Kumar V, Abbas AK, Fausto N, eds. Pathologic Basis of Disease. Philadelphia: Elsevier; 2005:1327.   7. Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice. 2nd ed. Philadelphia, FA: Davis; 1989.   8. Jin P, Min JC, et al. Local anesthetics. In: Dunn PF, Alston TA, Baker KH, eds. Clinical Anesthesia Procedures of the Massachusetts General Hospital. 7th ed. Philadelphia, Lippincott: Williams and Wilkins; 2007: 244.  9. Heavner JE. Pharmacology of local anesthetics. In: Longnecker DE, Brown D, Newman M, Zapol W, eds. Anesthesiology. New York: McGraw Hill; 2008:964. 10. Brown RS, Rhodus NL. Epinephrine and local anesthesia revisited. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2005;100(4):401-408. 11. Nolte J. Sensory receptors and the peripheral nervous system. In: Nolte J, The Human Brain, eds. An Introduction to Its Functional Anatomy. St. Louis: Mosby; 2002:219–220.

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242  Peripheral Nerve Blocks 12. Hafner HM, Rocken M, Breuninger H. Epinephrine-supplemented local anesthetics for ear and nose surgery: Clinical use without complications in more than 10,000 surgical procedures. J Dtsch Dermatol Ges. 2005;3(3):195-199. 13. Lalonde D, Bell M, Benoit P, et al. A multicenter prospective study of 3,110 consecutive cases of elective epinephrine use in the fingers and hand: The Dalhousie Project clinical phase. J Hand Surg Am. 2005;30(5): 1061-1067. 14. Thomson CJ, Lalonde DH, Denkler KA, Feicht AJ. A critical look at the evidence for and against elective epinephrine use in the finger. Plast Reconstr Surg. 2007;119:260-266. 15. Rosenberg PH, Veering BT, Urmey WF. Maximum recommended doses of local anesthetics: A multifactorial concept. Reg Anesth Pain Med. 2004;29(6):564-575. 16. Pasvankas GW, Sidhu DS, et al. Regional Anesthesia. In: Dunn PF, Alston TA, Baker KH, eds. Clinical Anesthesia Procedures of the Massachusetts General Hospital. 7th ed. Philadelphia, Lippincott: Williams and Wilkins; 2007:273. 17. Plevak DJ, Linstromberg JW, Danielson DR. Paresthesia vs. nonparesthesia: The axillary block. ASA Abstracts, Anesthesiology. 1983;59. 18. Selander D. Paresthesias or no paresthesias? Nerve complications after neural blockades. Acta Anaesthesiol Belg. 1988;39:173-174. 19. Selander D, Edshage S, Wolff T. Paresthesiae or no paresthesiae? Nerve lesions after axillary blocks. Acta Anaesthesiol Scand. 1979;23: 27-33. 20. Morgan GE, Mikhail MS, Murray MJ. Peripheral nerve blocks. In Mikhail MS, Murray MJ: Clinical Anesthesiology. 4th ed. New York: Lange/McGraw Hill; 2006:328. 21. Ilfeld BM, Enneking FK. A portable mechanical pump providing over four days of patient-controlled analgesia by perineural infusion at home. Reg Anesth Pain Med. 2002;27(1):100-104. 22. Boezaart AP. Perineural infusion of local anesthetics. Anesthesiology. 2006;104(4):872-880. 23. Mukherji SK, Wagle A, Armao DM, Dogra S. Brachial plexus nerve block with CT guidance for regional pain management: Initial results. Radiology. 2000;216:886-890. 24. Gentili F, Hudson A, Kline DG, Hunter D. Peripheral nerve injection injury: An experimental study. Neurosurgery. 1979;4:244-253. 25. Hudson AR. Nerve injection injuries. Clin Plast Surg. 1984;11:27-30. 26. Tsui BCH, Finucane BT. Managing adverse outcomes during regional anesthesia. In: Longnecker DE, Brown D, Newman M, Zapol W, eds. Anesthesiology. 1st ed. New York: McGraw Hill; 2008: 1060-1061.

26a. Selander D, Dhuner KG, Lundborg G. Peripheral nerve injury due to injection needles used for regional anesthesia. An experimental study of the acute effects of needle point trauma. Acta Anaesthesiol Scand. 1977;21:182-188.   27. Covino BG. Potential neurotoxicity of local anesthetic agents. Can Anaesth Soc J. 1983;30:111-116.   28. Selander D, Brattsand R, Lundborg G, et al. Local anesthetics: Importance of mode of application, concentration and adrenaline for the appearance of nerve lesions. An experimental study of axonal degeneration and barrier damage after intrafascicular injection or topical application of bupivacaine (Marcain). Acta Anesthesiol Scand. 1979;23: 127-136.   29. Selander D, Sjostrand J. Longitudinal spread of intraneurally injected local anesthetics. An experimental study of the initial neural distribution following intraneural injections. Acta Anaesthesiol Scand. 1978;22: 622-634.   30. Gentili F, Hudson AR, Hunter D, Kline DG. Nerve injection injury with local anesthetic agents: A light and electron microscopic, fluorescent microscopic and horseradish peroxidase study. Neurosurgery. 1980;6:263-272.   31. Myers RR, Kalichman MW, Reisner LS, Powell HC. Neurotoxicity of local anesthetics: Altered perineurial permeability, edema, and nerve fiber injury. Anesthesiology. 1986;64:29-35.   32. Mackinnon SE, Hudson AR, Gentili F, et al. Peripheral nerve injection injury with steroid agents. Plast Reconstr Surg. 1982;69:482-490.   33. Hebl JR, Horlocker TT, Pritchard DJ. Diffuse brachial plexopathy after interscalene blockade in a patient receiving cisplatin chemotherapy: The pharmacologic double crush syndrome. Anesth Analg. 2001;92:249-251. 33a. Choi YK, Liu J. The use of 5% lidocaine for prolonged analgesia in chronic pain patients. A new technique. Reg Anesth Pain Med. 1998;23:96-100. 33b. Fouch RA, Abram SE, Hogan QH. Neural blockade for upper extremity pain. Hand Clin. 1996;12:791-800.   34. Brown DL. Somatic or sympathetic block for reflex sympathetic dystrophy. Which is indicated? Hand Clin. 1997;13:485-497.   35. Moritz U. Phenol block of peripheral nerves. Scand J Rehabil Med. 1973;5:160-163.   36. Smith HM, Jacob AK, Segura LG, et al. Simulation education in ­anesthesia training: A case report of successful resuscitation of bupivacaine-induced cardiac arrest link to recent simulation training. Anesth Analg. 2008;106(5):1581-1584.

Ultrasound-Guided Nerve Blocks

24

Peter Stefanovich, MD

The use of ultrasound guidance to perform nerve blocks has been the most exciting development in the field of regional anesthesia in recent years. Instead of blindly advancing the needle toward the target nerve using anatomic landmarks, nerve stimulator, or paresthesia technique, the needle can now be advanced toward its target while imaging both the nerve and the advancing needle. This helps the operator appreciate variations in anatomy and identify structures such as blood vessels or the pleura that should be avoided while advancing the needle. Furthermore, local anesthetic spread around the nerves can be imaged in real time during performance of the block, which can help improve block quality (Fig. 24-1). Also, intraneural and intravascular positioning of the block needle can be identified early, thereby avoiding severe injury.1-3 To successfully use this technique, the detailed knowledge of cross-sectional anatomy, significant skill in advancing the needle, and experience in interpreting the ultrasound images is required. This requires the knowledge of artifacts of ultrasound-guided regional anesthesia such as acoustic enhancement and shadowing (Fig. 24-2).4 In addition, an understanding of basic ultrasound technology is needed to successfully practice ultrasound-guided regional anesthesia.5 The objective of this chapter is to introduce pain management physicians to ultrasound-guided nerve blocks. Although ultrasound guidance for pain management has only recently gained popularity, pain physicians are using this modality more frequently, sometimes in combination with fluoroscopic guidance. Although the block descriptions in this chapter are for regional anesthesia, we believe that the principles are the same when performing these or other peripheral nerve blocks for pain management. Also, we do not recommend abandoning older approaches such as nerve stimulator or paresthesia techniques; instead, we suggest using the ultrasound image as additional information to safely guide your needle toward the target nerve. Clinical practice has shown that intraneural positioning of a needle may not always cause a paresthesia or even nerve stimulation, particularly in diabetic patients.6 A paresthesia or the presence of motor stimulation using a nerve stimulator may alert you that your needle is too close to the nerve when the needle is poorly imaged with ultrasound. In this chapter, we will therefore also describe the role of nerve stimulation and eliciting paresthesias while performing the various nerve blocks (Fig. 24-3). We recommend reading specific books on ultrasound and gaining a detailed introduction on the specific ultrasound scanner you are using because this topic goes well beyond the scope of this chapter.

Some Brief Facts Ultrasound is a name given to high-frequency sound waves; 20,000 cycles per second (20 kHz) or higher, inaudible to human ears, that can be transmitted in beams and can be used to scan tissues of the body. Transducers emit ultrasound waves of different frequencies. Frequencies used for nerve blocks usually range from 5 to 14 MHz. The higher the frequency, the shorter the wavelength, the better the resolution. However, higher frequencies are more readily scattered and absorbed and therefore have poorer penetration of the tissue. Thus, for imaging of superficial structures (e.g., axillary nerve block, interscalene nerve block, vascular access) a high frequency transducer should be used. Lower frequency transducers will have better penetration of the tissue but have poorer resolution and should be used for nerves that are embedded deeper in the tissue (e.g., popliteal, infraclavicular, sciatic nerve block). This general rule is not written in stone, for example, you may be better off using a lower frequency when doing an interscalene nerve block in an obese patient and a high frequency could be used when doing a popliteal nerve block in a thin patient. In other words, the frequency should be adjusted according to the type of nerve block being performed and the patient’s body habitus. The transducers both transmit and receive ultrasound beams. The reflected ultrasound beams are received by the transducer and are amplified in the scanner. Different tissues alter the waves in different ways. Some scatter, whereas others reflect the waves directly before they return to the transducer as echoes. Bone and gas significantly reflect and scatter the ultrasound waves, whereas fluids produce a weak echo. Strong echoes appear as bright dots or lines on the screen and weak echoes appear as dark areas. The echoes that return from deeper structures are weaker than those from superficial structures and need to be amplified, which is done by the time-gain-compensation amplifier. After picking the appropriate frequency and depth setting you may be able to improve your image prior to starting the nerve block by adjusting the gain. Another useful function of the scanner is Doppler ultrasound. It can be used to detect blood flow in peripheral vessels and help avoid vascular injury while advancing the needle toward the target nerve. For this reason we recommend using the Doppler function to identify vessels close to the nerve before beginning any nerve block. 243

244  Peripheral Nerve Blocks

The two types of transducers typically used for nerve blocks are linear array (Fig. 24-4) and microconvex (curvilinear) transdu­ cers (Fig. 24-5). The linear array transducer emits high frequency ultrasound beams as the name states in a linear array and produces scans of rectangular shape. These transducers have a larger footprint than the microconvex probes and are better for scanning superficial structures (e.g., axillary nerve block, interscalene nerve block). The microconvex transducer has a small footprint and produces scans that are fan-shaped. Thus, larger sections of deeper tissue can be scanned compared to the linear array transducer. The microconvex probes usually also emit lower frequency ultrasound

Figure 24-3  Combining a nerve stimulator, as shown, with ultrasound guidance is recommended particularly when the nerve is poorly visualized.

Linear array La Sc

La

La: Local anesthetic Sc: Sciatic nerve Figure 24-1  Circumferential spread of local anesthetic around the sciatic nerve “doughnut sign.”

flata

fil

II II

fa

pen

fn

lateral

pen: posterior enhancement fil: fascia iliaca fa: femoral artery (ultrasound artifact) flata: facia lata fn: femoral nerve Figure 24-2  Ultrasound scan of the femoral nerve using a high-frequency linear array transducer. The needle should penetrate the fascia lata and the fascia iliaca for the block to be successful.

Figure 24-4  Linear array ultrasound transducer with rectangular scan.

Ultrasound-Guided Nerve Blocks  245

waves. It is therefore used to scan deeper structures (e.g., popliteal nerve block, infraclavicular nerve block) or in cases where only a small space is available for scanning (due to its smaller footprint). To successfully perform an ultrasound-guided nerve block, the nerve structures that are to be blocked and the structures that should be avoided, such as pleura and blood vessel, need to be

Microconvex

clearly identified. The ultrasound probe is typically placed where the needle insertion point would be in a conventional block technique. The needle is then inserted several centimeters from the probe site and advanced in plane of the ultrasound beam (Fig. 24-6). This allows continuous visualization of the needle as a hyperechoic (white) line. This is sometimes challenging particularly when blocking nerves in deeper tissues. However, it is of paramount importance for safely performing the block to image the needle clearly, particularly the needle tip. The needle can easily veer out of plane while advancing, which can lead to significant misjudgment of the location of the needle tip (Fig. 24-7). If this should occur we recommend pulling the needle back to just under the skin and then re-advancing it. Optimal imaging

Needle tip Nerve

Blood vessel

Figure 24-5  Microconvex ultrasound transducer with fan-shaped scan.

A

B

Figure 24-6  Demonstration of the in-line needle advancement technique using a linear array transducer and the “blue phantom gel model”. The needle is imaged in its entirety with the needle tip in close proximity to the nerve.

Figure 24-7  Using the in plane needle advancement technique as shown in Figure 24-6. The needle is placed intravascularly. A, intravascular position of the needle in the “blue phantom” model. B, same needle position as on the right, however, the ultrasound probe is placed out of plane. The virtual needle tip appears far away from the vessel. The real needle tip is, in fact, intravascular.

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246  Peripheral Nerve Blocks

Role of needle angle using “in plane” technique

Figure 24-8  The needle can be imaged more easily at a flatter angle. We recommend imaging the needle at a flat angle before advancing the it toward the target nerve at a steep angle, particularly when blocking nerves in deep locations.

of the needle may also require moving the ultrasound transducer from side to side, tilting it, or rotating the probe using a slow and steady motion. In addition, the flatter the angle of approach, the more easily the needle can be visualized.7 It is sometimes helpful to image the needle at a flat angle before advancing the needle at the appropriate angle for the target nerve (Fig. 24-8).

Role of the Nerve Stimulator During Ultrasound-Guided Nerve Blocks Even under ultrasound guidance the needle may inadvertently make contact with the nerve causing a paresthesia or even nerve injury. This is particularly true for the novice or when the there is poor visualization of the needle or the nerve—such as in the case of nerve blocks in deeper tissues. Contact of the needle with the nerve or even intraneural positioning may not always cause a paresthesia. Special care must be taken when blocking larger nerves such as the sciatic nerve and in diabetic patients. We recommend using the nerve stimulator response as an additional signal that the needle is approaching the nerve. The nerve stimulator can be used to identify specific nerves when ultrasound imaging of the nerve and the surrounding anatomy is less then optimal. We recommend using the nerve stimulator set at a low mA (0.4 mA to 0.5 mA) to minimize unpleasant muscle stimulation while advancing the needle under ultrasound guidance.

Preparing for Ultrasound-Guided Nerve Block Before performing an ultrasound-guided nerve block the skin needs to be prepped with an alcohol solution and the ultrasound probe should be covered with a sterile drape. For teaching purposes, the sterile cover is not shown in the following images because this would obscure the transducer position. Then, an ultrasound transducer

needs to be selected. For very deep structures, a microconvex or a low-frequency linear transducer should be used and for superficial structures, a linear transducer should be chosen. Next, the frequency on the scanner needs to be adjusted (e.g., 10 to 14 mHz for superficial structures, or 5 to 9 mHz for deep scanning). Subsequently the depth on the scanner needs to be set to about 1 to 2 cm deeper than the suspected nerve depth because the image size of the area of interest will be amplified if your depth setting is optimized. Now the gain (amplification) of your ultrasound signal should be adjusted which will frequently improve the image quality and give you better contrast. Always perform the blocks in a comfortable position for the patient and yourself (e.g., sitting position).8 Adjust the bed height so that your back is straight and your arms are bent at an approximately 90-degree angle at the elbows with both hands resting slightly at the wrist level on the patient. Hold the ultrasound probe at its base in your nondominant hand. Rest the ultrasound probe only very slightly on the body of the patient because compression of the tissue above the nerve may obscure the image of vessels close to the nerve, with possible accidental intravascular injection of local anesthetic.9

Upper Extremity Nerve Blocks Interscalene Nerve Block This nerve block is used for shoulder surgery as nerve roots C5, C6, C7 are blocked, including the suprascapular nerve, which supplies the glenohumeral joint of the shoulder (this is not blocked in supra-and infraclavicular nerve blocks.) Also nerve roots C8 and T1 are usually not blocked leading to ulnar sparing. It is performed with the patient in the half-lateral position with the patient’s head turned to the opposite side of the bed (Fig. 24-9). The ultrasound scanner is placed on the contralateral side of the bed. We recommend using an intermediate-to-high frequency (10 to 12 MHz) linear array probe set to a depth of 3 to 4 cm (2.5 cm in thin patients). It is placed above the clavicular head of the sternocleidomastoid muscle at the level of the cricoid cartilage (C6) where the internal jugular vein and carotid artery can easily be identified. The probe is now moved laterally and the anterior and middle scalene muscles are identified. The roots appear as round to oval hypoechoic structures located between the scalene muscles (Fig. 24-10).10 If you cannot identify the roots, move the transducer along an imaginary line made by the interscalene groove in a caudal direction and identify the nerve trunks or divisions in the supraclavicular area. Then follow the nerves back up to the C6 level. At this point we recommend using Doppler ultrasound to identify vascular structures close to the nerve roots because nerve roots and blood vessels appear very similar on the ultrasound image. After centering the nerve roots on the screen and infiltration of the skin with local anesthetic, a 22-gauge, 50 mm needle is inserted 1 to 2 cm lateral to the transducer. The needle is then advanced in plane to the probe through the middle scalene muscle. A distinct pop may be felt and tissue recoil may be seen when the needle enters and exits the middle scalene muscle. The needle tip should end up either between the C5 and C6 or the C6 and C7 nerve roots. Nerve stimulation can be used to confirm that the needle is not too close to the roots. After negative aspiration, 15 to 20 mL of local anesthetic is injected and the hypoechoic spread of local anesthetic around the roots should be visualized on the ultrasound image (Fig. 24-11).

Ultrasound-Guided Nerve Blocks  247

24 st C5

II

C6 as

C7

II

ms lateral st: sternocleidomastoid m. as: Anterior scalene m. ms: middle scalene m. Figure 24-9  The interscalene nerve block is performed with the patient in half-lateral position with the head turned to the opposite side of the bed.

C7

C6

Figure 24-10  Ultrasound scan of the interscalene groove using a high frequency linear array transducer.

II

II

C5

La

Needle

Needle

II

II

La: Local anesthetic

Supraclavicular Nerve Block The supraclavicular nerve block is sometimes referred to as the “spinal of the brachial plexus” because of the rapid onset of this dense block. The brachial plexus is blocked at the trunk or division level and is used for surgery of the hand or arm. It is performed with the patient in the half-lateral position with the patient’s head turned to the opposite side of the bed (Fig. 24-12). A high frequency 10 to 14 MHz linear array transducer is placed parallel to the clavicle at a depth setting of 2 to 4 cm. By tilting the probe in a caudad direction, the first rib, pleura, and the subclavian artery can easily be identified. The divisions of the brachial plexus have the appearance of a bunch of grapes at this level and are located lateral superior to the subclavian artery (Fig. 24-13). After infiltration of the skin with local anesthetic a 22-gauge, 50 mm needle is inserted 1 to 2 cm lateral to the transducer. Under ultrasound guidance, the needle is advanced toward the corner formed by the subclavian artery and the first rib (eight-ball corner pocket).11 Injection of 15 to 25 mL of local anesthetic at the corner pocket location will lead to circumferential spread of local anesthetic around the plexus. To advance the needle tip to the corner position, it may be

Figure 24-11  Local anesthetic spread around the cervical nerve roots seen as “dark” hypoechoic areas.

necessary to gently inject 3 to 5 mL of local anesthetic while at the 5 o’clock position to displace the plexus in the cephalad direction. To prevent puncturing the pleura, the hyperechoic line formed by the first rib should never be crossed by the needle. In patients with poor pulmonary function, this block should be used with caution because the incidence of pneumothorax and phrenic nerve block is comparatively high.

Infraclavicular Nerve Block The medial, lateral and posterior cords of the brachial plexus are blocked with this technique. It is indicated for surgery of the arm below the midhumerus as the axillary nerve is often spared. When compared to the supraclavicular nerve block, this block is bettersuited for patients with poor pulmonary function because it does not block the phrenic nerve and the incidence of pneumothorax is low. The patient is positioned supine with the arm abducted 90 degrees at the shoulder and the head slightly turned to the contralateral side (Fig. 24-14). The scanner is set to a depth of ~4 cm, depending on the patient’s body habitus, and placed on the contralateral side of the patient. Alternatively, the operator can sit at the

248  Peripheral Nerve Blocks

Figure 24-12  The supraclavicular nerve block is performed with the patient in half-lateral position with the patient’s head turned to the opposite side of the bed.

Figure 24-14  The infraclavicular block is performed with the patient in the supine position with the head turned to the opposite side of the bed and the arm slightly abducted.

II II

First rib

sa

II

* Pleura

mc av

sa: subclavian artery

II

pm

aa pc

lc

pm: pectoralis major m. av: axillary vein aa: axillary artery mc: medial cord lc: lateral cord pc: posterior cord

Figure 24-13  Ultrasound scan of the supraclavicular area using a high frequency linear array transducer. Notice the proximity of the pleura to the needle injection site.

head of the bed with the scanner placed on the ipsilateral side of the patient. Preferably, a mid- to low-frequency linear array transducer 6 to 9 MHz or microconvex low-frequency transducer is then placed ~2 cm below the cricoid process, in a plane parallel to the axis of the patient’s body, to obtain a good cross-sectional image of the axillary artery and vein (Fig. 24-15). The transducer can be rotated slightly medial to assess the distance of the pleura to the imaging plane (Fig. 24-16). A 22-gauge, 80 mm needle is then inserted ~2 cm cephalad to the transducer advancing the needle in plane, parallel to the plane of the patients body, never directing the needle medially toward the patient’s lung. The needle should be advanced between the lateral cord and the axillary artery toward the 5 or 6 o’clock position of the artery. One third of the local anesthetic should be injected at this position and spread of local anesthetic should be observed toward the medial cord between the artery and the vein. Another one third should be injected at the 4 o’clock, and another one third at the 3 o’clock position. If no spread toward the medial cord is observed, the needle should be withdrawn and advanced toward the medial cord

Figure 24-15  Ultrasound scan of the infraclavicular area using a low-frequency linear array probe. Notice the close proximity of the needle to the axillary artery.

located between the artery and the vein.12 A nerve stimulator set at 0.4 mA can be used as an additional safety factor to avoid injury of the lateral cord while advancing the needle between the lateral cord and axillary artery toward the 5 o’clock position of the artery.

Axillary Nerve Block The axillary nerve block is indicated in very sick patients with impaired blood coagulation (blood vessels can be easily compressed if injured by the needle) in which general anesthesia would be too risky. In addition, the axillary nerve block is indicated in patients with poor pulmonary function in whom phrenic nerve block and or pneumothorax (supra- or infraclavicular block) would be poorly tolerated. Axillary nerve block may be a good alternative in obese

Ultrasound-Guided Nerve Blocks  249

u

aa av Pleura

Resolution Freq 9.0MHz Depth 4cm Sector 60% Gain 54% FR high FPS 53 Hz Dyn 78dB Persist 2 Map 5 Chroma 0 Power –2 MI<0.92 Clarity high

Inferior

1

Figure 24-17  For the axillary nerve block, the operator is positioned at the head of the bed with the scanner placed on the same side of the bed.

patients in whom the brachial plexus can be poorly imaged in the supra- or infraclavicular location. The operator should sit at the head of the bed with the ultrasound scanner positioned on the side of the block. A high-frequency (12 to 14 MHz) linear array probe set at a depth of 2 to 3 cm is placed on the lateral wall of the axilla (Fig. 24-17). The axillary artery and vein are then located and centered in the middle of the screen. To avoid intravascular injection, hold the ultrasound probe gently against the skin surface because the axillary vein can be easily compressed by the probe and be missed on the ultrasound image. Always use Doppler ultrasound to identify blood vessels in the axilla because their anatomic location may vary considerably. A 22-gauge, 50 mm needle is then inserted 1 to 2 cm superior to the transducer and advanced in plane toward the artery. Three injections usually need to be made: One at the 11 o’clock position and one at the 5 o’clock position of the axillary artery leading to circumferential spread of local anesthetic around the artery, thereby blocking the ulnar, median, and radial nerves (Fig. 24-18). The injections need to be made very close to the axillary artery in order to achieve local anesthetic spread within the

Superior

3

mus av

ul

aa

med

rad

The pleura can be imaged by rotating the ultrasound transducer medially Figure 24-16  Ultrasound scan of the infraclavicular area using a lowfrequency microconvex transducer. The pleura should be imaged to access its relative distance to the block target.

2

Posterior av: axillary vein aa: axillary artery

ul: ulnar nerve rad: radial nerve

med: median nerve mus: musculocutaneous nerve

Figure 24-18  Ultrasound scan of the axillary area using a high-frequency linear array probe. Notice that injections at three different locations are required for a successful block.

Figure 24-19  Needle and transducer positioning for median nerve block.

nerve sheath. A third injection of 3 to 5 mL of local anesthetic is made next to the musculocutaneous nerve without changing the needle entry site. It has an oval to triangular hyperechoic appearance and can be easily visualized between the coracobrachialis and biceps muscles.

Median, Ulnar, and Radial Nerve Block Blocks of the median, ulnar, and radial nerves are usually performed as rescue blocks for incomplete supra-/infraclavicular and axillary nerve blocks or for surgery that is limited to the dermatomes of the individual nerves. At the wrist, the median nerve is located deep between the palmaris longus tendon and the flexor carpi radialis tendon. Having the patient move the fingers may help you differentiate the nerve from the tendons while imaging. Using a high frequency (12 to 14 MHz) linear array or hockey stick probe set to 2 cm depth, a 22-gauge, 25 mm or 50 mm needle is advanced in plane to the nerve and 3 to 5 mL of local anesthetic is injected (Figs. 24-19 and 24-20). The ulnar nerve is located posterior to the flexor carpi radialis tendon and lateral to the ulnar artery (Figs. 24-21 and 24-22). The technique is similar to blocking the median nerve just described.

24

250  Peripheral Nerve Blocks

Medial

Lateral II flex

pal Median nerve

II

Radius pal: palmaris longus tendon flex: flexor carpi radialis tendon

Figure 24-23  The radial nerve block is performed with the patient in half-­lateral position with the arm resting on the abdomen flexed at a 90-degree angle.

Figure 24-20  Ultrasound scan of the median nerve using a high-frequency linear array transducer.

Medial

Lateral

II Radial nerve

II Humerus

Figure 24-21  Needle and transducer positioning during ulnar nerve block.

Lateral

Figure 24-24  Ultrasound scan of the radial nerve using a high frequency linear array transducer. Notice the proximity of the radial nerve to the humerus.

Medial II Ulnar nerve UA II

The radial nerve can be blocked with the patient lying in the half-lateral position with the arm flexed and pronated, and resting on the patient’s abdomen. The radial nerve is imaged at the distal third of the upper arm with the transducer placed on the lateral aspect of the triceps. The needle is advanced from lateral in plane to the transducer toward the radial nerve, which can be imaged as it travels to the anterior compartment of the forearm and 3 to 5 mL of local anesthetic is injected at this location (Figs. 24-23 and 24-24).

Lower Extremity Nerve Blocks Ulna

Femoral Nerve Block UA: Ulnar artery

Figure 24-22  Ultrasound scan of the ulnar nerve and artery using a highfrequency linear array transducer.

With the patient in the supine position, an intermediate to high frequency (10 to 12 MHz) linear array probe is placed below the inguinal ligament at the femoral crease (Fig. 24-25). A cross-sectional image of the femoral artery is obtained and the femoral nerve is located just

Ultrasound-Guided Nerve Blocks  251

24

Figure 24-25  The femoral nerve block is performed with the patient in the supine position with the ultrasound scanner placed on the opposite side of the bed.

lateral to the artery and centered on the ultrasound screen (see Fig. 24-2). Two fascial layers can be visualized as hyperechoic lines with ultrasound: the superficial fascia lata overlying the femoral vessels and the deeper fascia iliaca overlying the femoral nerve and the iliopsoas muscle. A 50 to 80 mm, 20-gauge needle is inserted 1 to 2 cm lateral to the probe and advanced in plane to the transducer. Along its way, the needle will penetrate the superficial fascia lata and the deeper fascia iliaca. Frequently, a distinct “pop” can be felt and tissue recoil can be seen on the ultrasound screen when the needle penetrates the fascial layers. Twenty to 30 mL of local anesthetic is injected at the 4 to 5 o’clock position of the nerve. To completely encircle the femoral nerve with local anesthetic, a second injection of local anesthetic at the 1 o’clock position sometimes is required.

Subgluteal Sciatic Nerve Block This block can be used for leg surgery in patients who will have a thigh tourniquet. With the patient in the prone position, a line is drawn between the greater trochanter and the ischial tuberosity (Fig. 24-26). From the midpoint of this line, a perpendicular line is extended 4 cm caudally. A low-frequency linear or microconvex probe should be placed at this point, thereby imaging the sciatic nerve in cross-section. Sometimes it may be necessary to identify the sciatic nerve in the popliteal fossa because it is consistently superior and lateral to the popliteal vein and artery at this level. Under ultrasound guidance the sciatic nerve can then slowly be followed cephalad to the subgluteal area. The sciatic nerve at this level has an oval- to disc-shaped appearance (Fig. 24-27). A 20-gauge, 80 mm nerve stimulator needle is then advanced from lateral in line to the transducer to the 5 o’clock and then the 11 o’clock position of the nerve to completely encircle it with local anesthetic (see Fig. 24-1).

Figure 24-26  The subgluteal sciatic nerve block is performed with patient in the prone position and the ultrasound scanner placed on the opposite side of the bed.

u 2

ScN

1

General Freq 6.0MHz Depth 5cm Sector 60% Gain 52% FR high FPS 23 Hz Dyn 78dB Persist 2 Map 5 Chroma 0 Power –2 MI<0.92 Clarity high

ScN: Sciatic Nerve Figure 24-27  Ultrasound scan of the sciatic nerve in the subgluteal region using a low frequency convex transducer. Notice that the sciatic nerve is disc shaped at this location as opposed to more round shaped in the popliteal fossa (see Figure 24-28).

Popliteal Fossa Sciatic Nerve Block The patient is placed in the prone position with several blankets placed below the patient’s foot so that the leg is flexed at the knee (Fig. 24-28). This will cause the sciatic nerve to appear more round on the ultrasound image. A low frequency (5 to 8 MHz) linear array or microconvex transducer is placed 2 to 3 cm

Figure 24-28  The sciatic nerve is blocked in the popliteal fossa with the patient in the prone position. Blankets should be placed under the patient’s leg causing leg flexion leading to a more round appearance of the nerve.

252  Peripheral Nerve Blocks

2

1

sn

pv

pn

tn

pa

pv pa: popliteal artery pv: popliteal vein sn: sciatic nerve

Lateral

Figure 24-29  Ultrasound scan of the sciatic nerve in the popliteal fossa. Notice that the popliteal vein is consistently medial and posterior to the nerve and the artery is medial and posterior to the vein. Identifying the   vessels can help locate the nerve in large patients.

caudal from the tip of a triangle formed by the popliteal crease, biceps femoris muscle, and semimembranous tendon. The popliteal vein and artery are located and imaged in cross-section on the ultrasound screen. The sciatic nerve appears as a hyperechoic round or oval structure that is located superficial and lateral to the popliteal vein. The popliteal vein is superficial and lateral to the popliteal artery (Fig. 24-29). When the sciatic nerve is located, it should be followed in the caudad and cephalad direction to find the point at which it divides into the tibial and the common peroneal nerves (Fig. 24-30). The tibial nerve is larger and is located medial to the common peroneal nerve. The sciatic nerve should be blocked just cephalad from this point. After infiltration of the skin with local anesthetic, a 20-gauge, 80 mm needle is inserted approximately 1 inch lateral from the transducer and advanced in plane toward the 5 o’clock position of the sciatic nerve. At this location 15 mL of local anesthetic is injected and another 15 mL should be injected at 11 o’clock to achieve circumferential spread around the nerve. In patients who are not able to lie in the prone position, the sciatic nerve can also be blocked with the patient in the supine position with the leg resting on a Mayo stand (Fig. 24-31).

Conclusion The use of ultrasound guidance for the performance of peripheral nerve blocks has revolutionized the area of regional anesthesia. With a decrease in ultrasound scanner size and cost and the improvement of image quality, ultrasonography has become an indispensable tool for nerve blocks for surgical anesthesia. No doubt, ultrasound imaging will play an increasing role in procedures for pain management because, unlike fluoroscopy, it allows

pa

tn: tibial nerve pn: common peroneal n. pv: popliteal vein pa: popliteal artery

Figure 24-30  Ultrasound scan of the tibial and common peroneal nerve in the popliteal fossa using a linear array transducer. Injecting local anesthetic at this location may lead to faster onset of the block as compared to blocking the sciatic nerve at a more proximal location.

Figure 24-31  In patients who cannot be placed in the prone position, the sciatic nerve block can be performed with the leg elevated on a Mayo stand and the ultrasound transducer placed below the leg. In general, positioning becomes less important with ultrasound-guided nerve blocks as compared to more traditional block techniques.

imaging of soft tissues such as nerves, muscle, and blood vessels. However, to use this technology effectively, detailed knowledge of ultrasound technology, needle advancement technique, and crosssectional anatomy is necessary. This chapter should provide a foundation for learning the principles and techniques for peripheral nerve blocks under ultrasound guidance.

Ultrasound-Guided Nerve Blocks  253

REFERENCES   1. Russon K, Blanco R. Accidental intraneural injection into the musculocutaneous nerve visualized with ultrasound. Anesth Analg. 2007; 105(5):1504-1505.   2. Robards C, Hadzic A, Somasundaram L, et al. Intraneural injection with low-current stimulation during popliteal sciatic nerve block. Anesth Analg. 2009;109(2):673-677.   3. Martinez Navas A. De la Tabla Gonzalez RO: Ultrasound-guided technique allowed early detection of intravascular injection during an infraclavicular brachial plexus block. Acta Anaesthesiol Scand. 2009;53(7):968-970.   4. Sites BD, Brull R, Chan VW, et al. Artifacts and pitfall errors associated with ultrasound-guided regional anesthesia. Part II: A pictorial approach to understanding and avoidance. Reg Anesth Pain Med. 2007;32(5):419-433.   5. Palmer PES. Manual of diagnostic ultrasound. World Health Organization; 1995.   6. Bigeleisen PE, Moayeri N, Groen GJ. Extraneural versus intraneural stimulation thresholds during ultrasound-guided supraclavicular block. Anesthesiology. 2009;110(6):1235-1243.

  7. Gray AT. Ultrasound-guided regional anesthesia: Current state of the art. Anesthesiology. 2006;104(2):368-373.   8. Sites BD, Spence BC, Gallagher JD, et al. Characterizing novice behavior associated with learning ultrasound-guided peripheral regional anesthesia. Reg Anesth Pain Med. 2007;32(2):107-115.   9. Robards C, Clendenen S, Greengrass R. Intravascular injection during ultrasound-guided axillary block: Negative aspiration can be ­misleading. Anesth Analg. 2008;107(5):1754-1755. 10. Chan VW. Applying ultrasound imaging to interscalene brachial plexus block. Reg Anesth Pain Med. 2003;28:340-343. 11. Soares LG, Brull R, Lai J, Chan VW. Eight ball, corner pocket: the optimal needle position for ultrasound-guided supraclavicular nerve block. Reg Anesth Pain Med. 2007;32(1):94-95. 12. Sandhu NS, Capan LM. Ultrasound-guided infraclavicular brachial plexus block. Br J Anaesth. 2002;89:254-259.

24

Suprascapular Nerve Block

25

Jatin H. Joshi, MD, and Aneesh K. Singla, MD, MPH

Anatomy of the Suprascapular Nerve The suprascapular nerve is a mixed motor and sensory peripheral nerve originating from the upper trunk of the brachial plexus, receiving contributions predominantly from C5 and C6 fibers with approximately 22% of individuals also receiving contributions from C4.1 The suprascapular nerve gives motor innervation to the supraspinatus and infraspinatus muscles. Additionally, the nerve gives sensory and proprioceptive innervation to the glenohumeral joint, acromioclavicular joint, subacromial bursa, and the scapula (Fig. 25-1). Although the suprascapular nerve receives afferents from up to 70% of the shoulder joint, it rarely carries cutaneous afferent fibers. Cadaveric studies have found that as many as 15% of individuals have a cutaneous branch of the suprascapular nerve supplying the proximal, lateral one-third of the arm.2,3 After arising from the upper trunk of the brachial plexus, the suprascapular nerve courses through the posterior triangle of the neck, anterior to the trapezius muscle and posterior to the inferior belly of the omohyoid muscle (Fig. 25-2). The nerve then traverses through the suprascapular notch where it lies beneath the superior transverse scapular ligament and in close relation to the posterior border of the clavicle. Proximal to entering the suprascapular notch, the superior articular branch of the suprascapular nerve gives off sensory fibers to the coracoclavicular and coracohumeral ligaments, the acromioclavicular joint, and the subacromial bursa.3-6 Within the suprascapular notch, the suprascapular nerve gives rise to two motor nerves to the supraspinatus muscle.2 The nerve then passes through the notch and continues inferiorly, wrapping around the lateral margin of the scapular spine and through the spinoglenoid notch. Here, the suprascapular nerve sends a sensory branch to the posterior glenohumeral joint capsule. The nerve subsequently travels around the scapular spine, passing through a tunnel created by the spine of the scapula and spinoglenoid ligament (inferior transverse scapular ligament). The spinoglenoid ligament is a fibrous connective tissue band which originates from the lateral border of the scapular spine and inserts at the margin of the glenoid process.6 After passing through this space, the suprascapular nerve terminates by sending two to four motor branches to the infraspinatus muscle. Anatomic associations of the suprascapular nerve play an important role in source of injury. Proximally, the nerve’s close relation to the inferior border of the clavicle makes it potentially vulnerable to clavicular injuries. It is also hypothesized that anatomic variation in the shape of the suprascapular notch may predispose individuals to proximal suprascapular nerve entrapment. Cadaveric

studies of adult scapulae have shown that the suprascapular notch can exist in six shapes. The U-shaped (48%) and V-shaped (3%) are most commonly associated with nerve entrapment.2,7 Additionally, morphologic deviations in the superior transverse scapular ligament, such as calcification and hypertrophy, are also associated with suprascapular nerve injury.2 The suprascapular nerve is prone to injury distally where it passes through the tunnel formed by the scapular spine and the spinoglenoid ligament. Adduction and internal rotation of the shoulder is thought to tense the spinoglenoid ligament and subsequently stretch the nerve.2,8 In cadaveric studies, the spinoglenoid ligament has been identified in variable prevalence (15% to 80% of individuals).2,9,10 Interestingly, the ligament has been shown to be present more frequently in males (87%) than in females (50%), representing the higher likelihood of volleyball shoulder in males.6

Pathophysiology Common sources of suprascapular nerve injury are trauma, overuse, mass lesions, and operative causes. Traumatic injury to the suprascapular nerve occurs typically from fractures of the scapula and clavicle, dislocation of the shoulder, and penetrating injury. The most common location of injury to the suprascapular nerve is proximally at the suprascapular notch, and distally at the spinoglenoid notch. The mechanism of suprascapular nerve injury here is usually by repetitive overhead motions of the shoulder. In what is termed the sling effect, depression and retraction or hyperabduction of the shoulder causes the nerve to become apposed to the inferior margin of the superior transverse scapular ligament proximally or submitted to traction injury as it wraps around the scapular spine distally at the spinoglenoid notch.2 The sling effect underscores the importance of the scapula in overhead shoulder motions, such as throwing. These upper limb movements, causing scapular protraction and retraction, ultimately cause tension on the suprascapular nerve and sheer stress. Consequently, many suprascapular nerve injuries are in athletes using repetitive overhead motions that stress the shoulder.2 Alternative movements of the shoulder are also associated with distal suprascapular nerve injury. Abduction and external rotation causes the medial border of the infraspinatus tendon, inducing a compression injury at the spinoglenoid notch.2,11 Adduction or internal rotation of the upper limb is thought to cause traction of the suprascapular nerve at the spinoglenoid notch.2,12 Fast, repetitive, eccentric contraction of the infraspinatus muscle, in what is 255

256  Peripheral Nerve Blocks

From IV C. V C. To longus colli and scaleni

To rhomboidei To join the phrenic

VI C. To longus colli and scaleni VII C. To longus colli and scaleni Long thoracic

Suprascapular To subclavius Lateral anterior thoracic

rd

er

al

Musculocutaneous

t La

co

VIII C.

d or

To longus colli I T. and scaleni From II T.

rc

io er

t

s Po

Axillary

rd

Medial anterior thoracic

l co

dia Me

Upper subscap. Radial Median Ulnar

Thoracodorsal Lower subscap.

Medial brachial cutaneous

Medial antebrachial cutaneous

Figure 25-1  Brachial plexus. (From Gray H: Anatomy of the Human Body. Philadelphia, Lea & Febiger, 1918).

Su

pr

as

p.

Suprascapular

Superior branch of axillary

or

in

Deltoid

m

In

fra

sp

in

at

us

aj or

Te r

es

Cutaneous branches

m es

Radial

s ep

ic Tr

Te r

Inferior branch of axillary

Nerve to teres minor

termed “volleyball shoulder”, causes injury to the suprascapular nerve at its terminal portion.13,14 Compression effects may also cause injury to the suprascapular nerve. Ganglion cysts are the most common source of mass effect and primarily arise secondary to trauma to the joint capsule (Fig. 25-3). Other masses, including sarcomas and bone cysts may cause a similar effect.2

Figure 25-2  Course of suprascapular nerve on right side. (From Gray, H: Anatomy of the Human Body. Philadelphia, Lea & Febiger, 1918).

Patients with suprascapular nerve injury are typically young male athletes between 25 and 35 years of age with usually insidious onset of dominant upper extremity pain. They present with dull, achy pain in the posterior aspect of the shoulder. Overhead motion of the extremity exacerbates these symptoms. Because the majority of the suprascapular nerve’s sensory fibers are located proximally, pain is more associated with injury to the proximal aspect of the

Suprascapular Nerve Block  257

25

Figure 25-3  Coronal T2-weighted magnetic resonance image of the right shoulder demonstrating a ganglion cyst (arrow). (From Cummins CA, Messer TM, Nuber GW: Suprascapular nerve entrapment. J Bone Joint Surg Am. 2000;82[3]:415-424.)

Figure 25-5  Markings on the left shoulder of a patient with “X” ­demonstrating site of needle entry for suprascapular nerve blockade. ­(Keskinbora K, Aydinli I: Long-term results of suprascapular pulsed radio­ frequency in chronic shoulder pain. Agri. 2009; 21[1]:16-21.)

the clavicle and scapular spine. Distal suprascapular nerve lesions will manifest as tenderness to palpation at the spinoglenoid notch on physical examination. Patients may also have weakness in external rotation of the shoulder, a function of the infraspinatus and teres minor muscles. Also observed is a weakness in abduction, a function of the supraspinatus muscle.

Indications for Block

Figure 25-4  Posterior aspect of the left shoulder of a patient with marked atrophy of the infraspinatus muscle. (From Cummins CA, Messer TM, Nuber GW: Suprascapular nerve entrapment. J Bone Joint Surg Am. 2000; 82[3]: 415-424.)

nerve. Consequently, injury to the nerve distally at the spinoglenoid notch or volleyball shoulder causing isolated injury or atrophy to the infraspinatus are more likely to be insidious in onset and without any notable symptoms.13 Weakness may also manifest initially. However, many patients are asymptomatic and are incidentally found to have atrophy of the supraspinatus and infraspinatus muscles.2 Physical examination of individuals with suprascapular nerve injury will show atrophy of the supraspinatus and infraspinatus muscles (Fig. 25-4). Patients with proximal lesions of the suprascapular nerve will present with tenderness to palpation between

Suprascapular nerve blocks (Fig. 25-5) are indicated for neuropathy of the suprascapular nerve, pain from mass effects of malignancies and cysts, postoperative shoulder pain, or to assist with shoulder range of motion during rehabilitation of patients with adhesive capsulitis.15 Patients with inflammatory disease, including rheumatoid arthritis and spondyloarthropathies, will benefit from nerve blockade.16,17 Athletes with chronic shoulder pain from overuse injury may also benefit from suprascapular nerve block. Patients with severe osteoarthritis of the glenohumeral joint who are not candidates for total shoulder joint replacement and who do not benefit from intraarticular corticosteroid injections are candidates for suprascapular nerve blockade for pain relief. Additionally, injection of a local anesthetic into the suprascapular notch has been found by some authors to be helpful in diagnosing suprascapular nerve entrapment by exclusion.2

Techniques for Suprascapular Nerve Block Suprascapular nerve blockade is accomplished by injecting local anesthetic solution around the suprascapular nerve at the suprascapular notch. The suprascapular notch is an ideal location for neural blockade, given the relative ease of accessibility for the operator. Additionally, at this level, the suprascapular nerve gives branches to the glenohumeral joint, the acromioclavicular joint, and the supraspinatus muscle.16 If done without fluoroscopy, the patient is placed in a sitting position with his or her back to the examiner and the hand of the affected side resting on the contralateral shoulder to help contour the shoulder and back in optimal position for a successful block. The procedure

258  Peripheral Nerve Blocks

Subcutaneous tissue

Subcutaneous tissue

Trapezius Trapezius

Supraspinatus Transverse scapular ligament

LA spread at needle tip Supraspinatus

Coracoid process

Suprascapular nerve

Figure 25-6  Transverse view of suprascapular fossa and scapular notch with a SonoSite ultrasound system and a 6-13 MHz linear transducer. (From ­Harmon D, Hearty C: Ultrasound-guided suprascapular nerve block ­technique. Pain Physician. 10:743-746. 2007.)

must be performed in a sterile manner and the skin must be cleansed with an antiseptic solution. The site of injection for nerve blockade is found by first identifying the spine of the scapula by palpation and drawing a line along the length of the scapular spine. The line should be in an oblique orientation, heading superiorly and laterally toward the acromion. At approximately the midpoint of this line, a second vertical line is drawn parallel to the vertebral spine. This line is intended to bisect the angle of the scapula superiorly and extend toward the tip of the scapula inferiorly. The upper outer quadrant formed by these two lines is further bisected with a third line. The injection site for suprascapular nerve blockade is approximately 2 cm along this third line.16,18,19 A subcutaneous wheal with lidocaine (Xylocaine) 1% solution is made to anesthetize the site of needle injection. A 22 gauge, 38 mm insulated block needle with a nerve stimulator is aligned parallel to the patient’s back at the point of injection. The needle is inserted through the skin toward the scapular spine. When contact with the spine is made, the block needle should be carefully directed anteriorly to enter into the suprascapular notch.19 A motor response by the supraspinatus and infraspinatus muscles to 0.3 to 0.5 mA and 0.1 msec confirms accurate needle position. When satisfactory needle position is obtained, the operator should always aspirate from the needle to ensure the needle is not in an intravascular space. ­Approximately 10 mL of 0.5% bupivacaine and 40 mg methylprednisolone or triamcinolone should be injected to fill the space around the nerve. The anesthetic agent should be injected slowly because rapid injection of anesthetic solution into this fixed space can cause trauma to the nerve.15,20 Because of the proximity of the suprascapular notch to the

Transverse scapular ligament

Figure 25-7  Real-time imaging of needle insertion for the ultrasound-guided suprascapular block (From Harmon D, Hearty C: Ultrasound-guided suprascapular nerve block technique. Pain Physician. 10:743-746. 2007.)

pleural cavity, pneumothorax may result if the block needle is placed too deep within the suprascapular notch. Ultrasound guidance can also be used for suprascapular nerve blockade, either alone or with a combined nerve stimulator technique. The technique is similar to that described earlier. Perineural spread of local anesthetic will appear as a hypoechoic shadow on ultrasound. Figures 25-6 and 25-7 outline ultrasound-directed views of the suprascapular nerve during nerve blockade. Fluoroscopic guidance for suprascapular nerve blockade facilitates identification of the anatomy and offers a higher chance for a successful intervention. The technique has potential safety advantages, including reduced risk of pleural injury and intravascular spread of local anesthetic. For fluoroscopy-guided blocks, patients are placed in prone position with the fluoroscopy unit angled in a caudocranial direction. The suprascapular notch is first identified anterior to the spine of the scapula (Fig. 25-8). A subcutaneous wheal with lidocaine (­Xylocaine) 1% solution is made to anesthetize the site of needle injection. A 25 gauge, 3.5 inch spinal needle is aligned parallel to the x-ray beam and positioned in the suprascapular notch, by first contacting the scapular spine and then by carefully directing the needle anteriorly to enter into the suprascapular notch.19 When satisfactory needle position is obtained, the operator should always aspirate from the needle to ensure it is not in an intravascular space, and 1 mL of nonionic contrast should be injected under continuous fluoroscopy to confirm spread along the suprascapular nerve and to rule out intravascular spread (Fig. 25-9). Approximately 10 mL of 0.5% bupivacaine and 40 mg methylprednisolone or triamcinolone should be injected to fill the contents of

Suprascapular Nerve Block  259

the suprascapular notch. Similar to the anatomic landmark approach, pneumothorax is a potential complication and the anesthetic agent should be injected slowly to prevent nerve trauma. REFERENCES

Figure 25-8  Suprascapular nerve block under fluoroscopy. Note needle tip placement in suprascapular notch.

Figure 25-9  Suprascapular nerve block under fluoroscopy. Note spread of nonionic contrast along suprascapular nerve.

  1. Lee HY, Chung IH, Sir WS, et al. Variations of the ventral rami of the brachial plexus. J Korean Med Sci. 1992;7:19-24.   2. Cummins CA, Messer TM, Nuber GW. Suprascapular nerve entrapment. J Bone Joint Surg Am. 2000;82(3):415-424.   3. Ajmani ML. The cutaneous branch of the human suprascapular nerve. J Anat. 1994;185:439-442.   4. Inouye Y. Conduction along the articular branch of the suprascapular nerve. Acta Neurol Scand. 1978;58:230-240.   5. Mestdagh H, Drizenko A, Ghestem P. Anatomical bases of suprascapular nerve syndrome. Ana Clin. 1981;3:67-71.   6. Lee BC, Yegappan M, Thiagarajan P. Suprascapular nerve neuropathy secondary to spinoglenoid notch ganglion cyst: Case reports and review of literature. Ann Acad Med Singapore. 2007;36:1032-1035.   7. Rengachary SS, Neff JP, Singer PA, Brackett CE. Suprascapular entrapment neuropathy: A clinical, anatomical, and comparative study. Part 1: Clinical study. Neurosurgery. 1979;5:441-446.   8. Demirhan M, Imhoff AB, Debski RE, et al. The spinoglenoid ligament and its relationship to the suprascapular nerve. J Shoulder Elbow Surg. 1998;7:238-243.   9. Ticker JB, Djurasovic M, Strauch RJ, et al. The incidence of ganglion cysts and other variations in anatomy along the course of the suprascapular nerve. J Shoulder Elbow Surg. 1998;7:472-478. 10. Cummins CA, Anderson K, Bowen M, et al. Anatomy and histological characteristics of the spinoglenoid ligament. J Bone Joint Surg Am. 1998;80:1622-1625. 11. Sandow MJ, Ilic J. Suprascapular nerve rotator cuff compression syndrome in volleyball players. J Shoulder Elbow Surg. 1998;7(5):516-521. 12. Demirhan M, Imhoff AB, Debski RE, et al. The spinoglenoid ligament and its relationship to the suprascapular nerve. J Shoulder Elbow Surg. 1998;7:238-243. 13. Ferretti A, De Carli A, Fontana M. Injury of the suprascapular nerve at the spinoglenoid notch. The natural history of infraspinatus atrophy in volleyball players. Am J Sports Med. 1998;26(6):759-763. 14. Ferretti A, Cerullo G, Russo G. Suprascapular neuropathy in volleyball players. J Bone Joint Surg Am. 1987;69(2):260-263. 15. Weiss JM, Lennard TA, Silver JK, Weiss LD. Easy Injections. New York: Elsevier Health Sciences; 2007. 16. Shanahan EM, Ahern M, Smith M, et al. Suprascapular nerve block (using bupivacaine and methylprednisolone acetate) in chronic shoulder pain. Ann Rheum Dis. 2006;62:400-406. 17. Shanahan EM, Ahern M, Smith M, et al. Suprascapular nerve block reduced chronic shoulder pain and disability in degenerative disease or rheumatoid arthritis. Evid Based Med. 2004;9:50. 18. Bockenek WL, Walsh NE, Gans BM, DeLisa JA. Physical medicine and rehabilitation: Principles and practice. Philadelphia: ­Lippincott ­Williams & Wilkins; 2004. 19. Argoff CE, Turk DC, Wu CL, et al. Raj’s Practical Management of Pain. New York: Elsevier; 2008. 20. Büttner J, Meier G. Peripheral Regional Anesthesia. New York: Thieme; 2007.

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26

Sciatic Nerve Block Karan Madan, MBBS, MPH, and Ajay D. Wasan, MD, MSc

Sciatic nerve blockade is useful for surgical anesthesia, postoperative pain for lower extremity surgery, and for management of pain in certain lower extremity chronic pain syndromes such as sciatic neuropathy. This chapter describes the anatomy, various block approaches, and potential complications of this procedure.

Anatomy The sciatic nerve is the largest nerve in the body and is found in the pelvis from the ventral rami of the fourth lumbar to the third sacral spinal nerves.1 It transverses through the sciatic foramen and below the piriformis to enter the lower extremity and then descends between the greater trochanter and the ischial tuberosity (Fig. 26-1). In some cases the common peroneal component may pass through the piriformis, whereas the tibial component passes below the muscle. The sciatic nerve runs down the posterior aspect of the thigh and divides into the common peroneal nerve and tibial nerve. During this course, it is accompanied by the posterior femoral cutaneous nerve and the inferior gluteal artery. Here it lies deep to the gluteus maximus—running in the posterior ischial surface. Further down it turns posterior to the obturator internus, the gemelli, and the quadratus femoris. Distally it lies behind the adductor magnus and the long head of biceps femoris crosses it posteriorly. It corresponds to a line drawn from just medial to the midpoint between the ischial tuberosity and the greater trochanter to the apex of the popliteal fossa. There is considerable variation in the level of the division of the sciatic nerve into the common peroneal nerve and the tibial nerve because they are usually connected by a thin fascial plane. The sciatic nerve innervates the hip joint through the posterior capsule, the knee joint, and all the hamstring muscles. This nerve also supplies the muscles of the posterior compartment of the leg.

History Historically, the sciatic nerve block was first described by Victor Pauchet in 1920. In 1923, a similar approach was described by Gaston Labat in his book, Regional Anesthesia: Its Technique and Clinical Application. In 1975, Alon Winnie described the “modified Labat” technique. The anterior approach to the sciatic nerve block was described by Beck. In 1993, Mansour described the parasacral approach to the sacral plexus.2 Di Beneditto and ­colleagues described the subgluteal approach to the sciatic nerve block in 2001.3

Indications for Sciatic Nerve Block Sciatic nerve block is indicated for lower limb surgery including surgery on the knee, ankle, and foot. A lumbar plexus block is beneficial for hip surgery. Various studies have demonstrated the benefits of continuous popliteal (sciatic nerve) block for postoperative pain control after painful orthopedic foot surgery. The benefits include decreased pain, reduced opioid requirements and opioid-related adverse effects.4-6 Sciatic nerve block may be a useful adjunct for certain lower extremity chronic pain syndromes such as sciatic neuropathy or piriformis syndrome where there is compression of the sciatic nerve at the piriformis muscle.

Sciatic Nerve Block—Posterior Approach Patient is positioned in the lateral decubitus position. Surface anatomical landmarks for posterior approach are: 1. Posterior superior iliac spine 2. Greater trochanter of femur The needle insertion site is 4 cm below the midpoint of the line joining the posterior superior iliac spine (PSIS) to the ipsilateral greater trochanter (Fig. 26-2). The needle is inserted perpendicular to the skin. A nerve stimulator with a standard setting of 2 Hz and 100 μsec can be used and will initially cause a twitching of the gluteal muscles. On further advancement of the needle and with stimulation of the sciatic nerve, contraction of the hamstrings and calf muscles will be noted. This is observed as dorsiflexion of the ankle and foot. Small adjustments of the needle may become necessary to achieve stimulation at less than 0.5 mA. The stimulation current may be reduced until disappearance of stimulation is noted. This should usually be above 0.2 mA. After initial and intermittent negative aspiration 15 to 30 mL of local anesthetic is injected in increments of 4 to 5 mL. Injection of local anesthetic should be without any resistance and without pain or paresthesia. Triamcinolone (40 to 80 mg) or other corticosteroid with a lower volume of local anesthetic can be added when used for treatment of chronic pain syndromes. In situations where prolonged postoperative analgesia is required, a catheter is threaded 5 to 10 cm beyond the needle tip and left in situ. Prior to injecting local anesthetic through the catheter, it should always be aspirated to confirm that the catheter tip is not intravascular. 261

262  Peripheral Nerve Blocks

Sciatic Nerve Block—Anterior Approach The patient is positioned in the supine position. The leg is maintained fully extended. If the patient has an overhanging abdominal pannus, it may need to be either held up or taped to fully expose the inguinal area and femoral crease of the patient. L2

Lateral femoral cutaneous nerve

L3 L4

Femoral nerve

L5

S1 S2 Piriformis muscle

S3 Obturator nerve

Surface anatomic landmarks for anterior approach are the femoral crease and the femoral artery pulse. The femoral artery is palpated within the femoral crease. From this point, a line is drawn perpendicular to the femoral crease to identify a point 5 cm distal to the femoral crease (Fig. 26-3). At this point, a needle is inserted perpendicular to the skin plane. A nerve stimulator with a standard setting of 2 Hz and 100 μsec can be used and will initially cause contraction of the quadriceps muscles. On further advancement of the needle and stimulation of the sciatic nerve, contraction of the hamstrings and calf muscles will be noted. Make small adjustments of the needle if necessary to achieve stimulation at less than 0.5 mA. Continue to reduce the stimulation current until the contraction disappears. This should usually be above 0.2 mA. After initial and intermittent negative aspiration of blood 15 to 30 mL of local anesthetic can be injected in increments of 4 to 5 mL. Injection of local anesthetic should be without any resistance and without pain or paresthesia. If bone was contacted prior to obtaining the desired stimulation, the needle can be reinserted medially. Triamcinolone (40 to 80 mg) or other corticosteroid with a lower volume of local anesthetic can be added when used for treatment of chronic pain syndromes.

Lumbar Plexus Block—Parasacral Approach

Ischial tuberosity Posterior Sciatic cutaneous nerve nerve

Greater trochanter of femur

Figure 26-1  Sciatic nerve anatomy. (From Brown DL: Atlas of Regional ­Anesthesia, 3rd ed. Philadelphia, Saunders, 2005.)

The parasacral approach to a lumbar plexus block was described by Mansour in 1993.7 This block can be used for anesthesia and analgesia in patients having lower extremity hip, tibia and fibula, knee, ankle, and foot surgery and amputation at the level of the knee.8 The patient is positioned in the lateral decubitus position. Surface anatomic landmarks for parasacral lumbar plexus block are the posterior-superior iliac spine and the ischial tuberosity. A line is drawn connecting the posterior-superior iliac spine and the ischial tuberosity. On this line, the needle is inserted

Greater trochanter

Piriformis muscle

Sciatic nerve

Posterior superior iliac spine

Ischial tuberosity

Figure 26-2  Sciatic nerve block: posterior approach. (From Brown DL: Atlas of Regional Anesthesia, 3rd ed. Philadelphia, Saunders, 2005.)

Sciatic Nerve Block  263

6 cm from the posterior superior iliac spine and advanced in the sagittal plane. A nerve stimulator with a standard setting of 2 Hz and 100 μsec can be used and will cause a contraction of the hamstring and posterior leg muscles. Make small adjustments of the needle position if necessary to achieve stimulation at less than 0.5 mA. Continue to reduce the stimulation current until the contraction disappears. This should usually be above 0.2 mA. After initial and intermittent negative aspiration 15 to 30 mL of local anesthetic can be injected in increments of 4 to 5 mL. Injection of local anesthetic should be without any resistance and without pain or paresthesia. If bone was contacted prior to obtaining desired stimulation, the needle should be redirected caudally. Triamcinolone (40 to 80 mg) or other corticosteroid with a lower volume of local anesthetic can be added when used for treatment of chronic pain syndromes.

Sciatic Nerve Block at the Popliteal Fossa The sciatic nerve consists of two separate nerve trunks—the tibial and common peroneal nerves (Fig. 26-4). These nerves share a common epineural sheath and are separated throughout their course by a thin fascial plane. In the popliteal fossa, the tibial and common peroneal nerves diverge. The level of this separation is highly variable and occurs from 5 to 12 cm proximal to the popliteal crease.9 The common peroneal nerve continues behind the

L4

fibular head and divides into the superficial and deep peroneal nerves. The superficial peroneal nerve innervates the lateral compartment muscles of the leg (peroneal longus and brevis). The deep peroneal nerve innervates the anterior compartment muscles of the leg. The tibial nerve travels down in the posterior aspect of the leg with the posterior tibial artery. During its course, it gives rise to the medial sural cutaneous and medial calcaneal branches. The tibial nerve terminates as the medial and lateral plantar nerves. To perform a sciatic nerve block at the popliteal fossa, the patient is positioned in the prone position. For patient comfort and improved visualization of the ankle, the ankle may be slightly elevated by placing a blanket under it. Surface anatomic landmarks for sciatic nerve block at the popliteal fossa include tendons of semitendinosus and semimembranosus muscles medially; the tendon of the biceps femoris muscle laterally; and the popliteal crease inferiorly. These landmarks are clearly identified and marked by asking the patient to flex the leg at the knee. The needle can be inserted at the midpoint between the tendons about 7 to 10 cm proximal to the popliteal crease. A nerve stimulator with a standard setting of 2 Hz and 100 μsec can be used. Stimulation of the common peroneal nerve will result in dorsiflexion and eversion at the ankle, whereas stimulation of the tibial nerve results in plantar flexion and inversion at the ankle. Either of these responses is acceptable. Make small adjustments of the needle if necessary to achieve stimulation at less than 0.5 mA. Continue to reduce the stimulation current until the contraction subsides. This should usually be above 0.2 mA. After initial and intermittent negative aspiration, 25 to 30 mL of local anesthetic is injected in increments of 4 to 5 mL. Injection of local anesthetic should be without any resistance and without pain or paresthesia. Triamcinolone (40 to 80 mg) or other corticosteroids with a lower volume of local anesthetic can be added when used for treatment of chronic pain syndromes.

L5 PROXIMAL S1 S2 Anterior superior iliac spine Greater trochanter

LATERAL

MEDIAL

1/3

S3

1/3

Tibial nerve Pubic tubercle

Interosseus nerve of leg Sural nerve Common peroneal nerve Deep branch Superficial branch

NEEDLE INSERTION SITE Sciatic nerve

DISTAL Figure 26-3  Sciatic nerve block: landmarks for anterior approach. (From Brown DL: Atlas of Regional Anesthesia, 3rd ed. Philadelphia, Saunders, 2005.)

Figure 26-4  Sciatic nerve anatomy in the popliteal fossa. (From Brown DL: Atlas of Regional Anesthesia, 3rd ed. Philadelphia, Saunders, 2005.)

26

264  Peripheral Nerve Blocks

The needle is visualized as a hyperechoic circular structure and the full length of the needle is not visualized. If using this method, it may be helpful to combine the use of a standard nerve stimulator with a setting of 2 Hz and 100 μsec. Alternatively, the needle can be inserted laterally, parallel to the ultrasound probe, but anterior to the tendon of the biceps femoris. With this approach, the entire length of the needle can be visualized under ultrasound. When the needle is in appropriate proximity of the sciatic nerve, plantar or dorsiflexion of the foot will be noted with less than 0.5 mA when a nerve stimulator is used. Either of these contractions is acceptable. Continue to reduce the stimulation current until disappearance of contraction is noted. This should usually be above 0.2 mA. After initial and intermittent negative aspiration 15 to 30 mL of local anesthetic is injected in increments of 4 to 5 mL. Injection of local anesthetic should be without any resistance and without pain or paresthesia. Spread of the local anesthetic around the sciatic nerve can be visualized on the ultrasound. Triamcinolone (40 to 80 mg) or other corticosteroids with a lower volume of local anesthetic can be added when used for treatment of chronic pain syndromes. Figure 26-5  Ultrasound image of dividing sciatic nerve in the popliteal fossa. (Image courtesy of Dr. Amir Islami.)

Sciatic Nerve Block under Ultrasound Guidance In a study performed by Perlas and colleagues, ultrasound guidance improved the success of sciatic nerve block at the popliteal fossa.10 This study showed the success rate for ultrasound-guided block was 89.2% versus a nerve stimulator-guided group with the success rate of 60.6%. Ideally, a lower frequency ultrasound probe between 2 and 5 MHz may be used for scanning and identifying deep structures such as the sciatic nerve.

Ultrasound-Guided Popliteal Sciatic Nerve Block Surface anatomic landmarks for sciatic nerve block at the popliteal fossa follow: 1. Tendons of semitendinosus and semimembranosus muscles medially 2. The tendon of the biceps femoris muscle laterally 3. Popliteal crease inferiorly The patient is positioned prone and the surface landmarks as described earlier are identified and clearly marked. The ultrasound probe is positioned 5 to 10 cm proximal to the popliteal crease to obtain a short axis or transverse view of the sciatic nerve.11 The sciatic nerve at this level will appear as a single circular or oval structure (Fig. 26-5). The popliteal artery appears as a hypoechoic pulsatile structure medial to the sciatic nerve. Attempt to visualize the sciatic nerve in the upper portion of the popliteal fossa prior to its division into the tibial and common peroneal nerves. The ultrasound probe should be moved cephalad until this point is located. Every effort should be made to visualize the sciatic nerve in the center of the sonogram. In the more commonly performed posterior approach, the needle is placed perpendicular to the center of the ultrasound probe.

Ultrasound-Guided Mid-thigh Sciatic Nerve Block12 Surface anatomic landmarks for posterior approach are posterior superior iliac spine and greater trochanter of femur. The patient is positioned in the prone position. This block may also be performed with the patient in a lateral position with the operative side up. A line is drawn that connects the posterior-superior iliac spine to the ipsilateral greater trochanter of the femur. A low-frequency ultrasound probe preferably 2 to 5 MHz may be used to scan from the midpoint of the line described earlier down to the popliteal crease with the goal to identify the sciatic nerve. The sciatic nerve should be visualized in the short axis. After anesthetizing the skin, the needle can be inserted just lateral to and parallel to the ultrasound probe. The needle can be advanced medially under direct vision on the sonogram. If a nerve stimulator is also used, contraction of the calf muscles along with plantar or dorsiflexion of the foot can be noted with less than 0.5 mA. The stimulation current can be reduced until the contraction subsides. This should be >0.2 mA. After initial and intermittent negative aspiration 15 to 30 mL of local anesthetic is injected in increments of 4 to 5 mL. Injection of local anesthetic should be without any resistance and without pain or paresthesia. Spread of the local anesthetic around the sciatic nerve can be visualized on the sonogram. Triamcinolone (40 to 80 mg) or other corticosteroid with a lower volume of local anesthetic can be added when used for treatment of chronic pain syndromes.

Sciatic Nerve Block with Fluoroscopic Guidance Using a slight modification of the posterior approach described earlier, the sciatic nerve can be blocked at the sciatic notch using fluoroscopic guidance. Using a 25- or 22-gauge 3.5 inch spinal needle, the sciatic notch can be targeted to access the sciatic nerve. As the needle is advanced parallel to the fluoroscopic x-ray beam, and the needle comes in contact with the sciatic nerve, a paresthesia will be elicited, or the procedure can be done with a nerve stimulator as described previously. As soon as the nerve is in proximity, 1 to

Sciatic Nerve Block  265

artery is located medial to the sciatic nerve and deeper to the nerve. Knowledge of the anatomy and good visualization under ultrasound guidance may also help avoid vascular puncture. Intravascular injection: Constant negative aspiration should be maintained during needle positioning and insertion. Prior to injection of local anesthetic, negative aspiration should always be performed to confirm that the needle is not placed intravascularly. Intermittent negative aspiration every 4 to 5 mL is also advised to avoid this complication because small movements are possible during local anesthetic injection. If continuous infusion is planned, it is very important to aspirate on the catheter to confirm that it is not placed intravascularly prior to injection through the nerve catheter. Other complications of the sciatic nerve block include a transient unintended pudendal nerve block, perforation of pelvic organs, and pressure necrosis of the heel.19,20

Conclusion

Figure 26-6  Sciatic nerve block under fluoroscopic guidance: posterior approach.

2 mL of nonionic contrast media is injected and an outline of the sciatic nerve is seen (Fig. 26-6). Local anesthetic with or without 40 to 80 mg triamcinolone or other corticosteroid can be injected after negative aspiration for blood.

Complications of Sciatic Nerve Block Various studies analyzed complications following peripheral nerve blocks.13,14 Recent studies have also examined complications after continuous popliteal sciatic nerve blocks for postoperative analgesia.15,16 Some of the following common complications have been observed during or after the performance of sciatic nerve blocks: Infection: The incidence of infection has ranged from 0.1% to 3.2% as reported by various studies.13,15,17 Longer duration of catheter insertion has been assumed to increase the incidence of infection; however, no definitive data are available to corroborate this assumption. Meticulous sterile prep, technique, and dressing have been shown to reduce the incidence of infection for central venous line catheters.18 We believe similar care would help avoid infections following the performance of peripheral nerve blocks. Nerve injury: The incidence of nerve injury has been reported between 0.21% and 0.5% with the sciatic nerve blocks.15 Mechanisms for nerve injury include the use of pneumatic tourniquet on the upper third of the leg and direct nerve injury from needle and injection trauma. Techniques to avoid potential nerve injury would include slow needle advancement, avoidance of forceful injections, and avoiding injecting when the patient is insensate. Vascular injury and hematoma: Vascular puncture and hematoma can be prevented by slow and meticulous movement and advancement of the needle, thereby avoiding multiple needle passes. In the popliteal fossa as mentioned earlier, the popliteal

Sciatic nerve blockade can be useful for surgical anesthesia, postoperative pain control, and for management of certain lower extremity chronic pain syndromes. Although sciatic nerve block has traditionally been performed without image guidance, an increasing number of practitioners are using ultrasound or fluoroscopic guidance to improve accuracy and to lower the risk of complications. REFERENCES   1. Williams A. Pelvic girdle gluteal region and hip joint area. In: Standring S, ed. Gray’s Anatomy: The Anatomical Basis of Clinical Practice 39th ed. Philadelphia: Elsevier; 2004.   2. Mansour NY. Reevaluating the sciatic nerve block: Another landmark for consideration. Reg Anesth. 1993;18:322-333.   3. di Benedetto P, Bertini L, Casati A, et al. A new posterior approach to the sciatic nerve block: A prospective, randomized comparison with the classic posterior approach. Anesth Analg. 2001;93:1040-1044.   4. Singelyn FJ, Aye F, Gouverneur JM. Continuous popliteal sciatic nerve block: An original technique to provide postoperative analgesia after foot surgery. Anesth Analg. 1997;84:383-386.   5. Ilfeld BM, Morey TE, Wang RD, Enneking FK. Continuous popliteal sciatic nerve block for postoperative pain control at home: A randomized, double-blinded, placebo-controlled study. Anesthesiology. 2002;97:959-965.   6. White PF, Issioui T, Skrivanek GD, et al. The use of a continuous popliteal sciatic nerve block after surgery involving the foot and ankle: Does it improve the quality of recovery? Anesth Analg. 2003;97:1303-1309.   7. Mansour NY. Reevaluating the sciatic nerve block: Another landmark for consideration. Reg Anesth. 1993;18:322-323.   8. Morris GF, Lang SA, Dust WN, Van der Wal M. The parasacral sciatic nerve block. Reg Anesth. 1997;22:223-228.   9. Vloka JD, Hadzić A, April E, Thys DM. The division of the sciatic nerve in the popliteal fossa: Anatomical implications for popliteal nerve blockade. Anesth Analg. 2001;92(1):215-217. 10. Perlas A, Brull R, Chan VW, et al. Ultrasound guidance improves the success of sciatic nerve block at the popliteal fossa. Reg Anesth Pain Med. 2008;33(3):259-265. 11. Sinha A, Chan VW. Ultrasound imaging for popliteal sciatic nerve block. Reg Anesth Pain Med. 2004;29(2):130-134. 12. Barrington MJ, Lai SL, Briggs CA, et al. Ultrasound-guided midthigh sciatic nerve block—a clinical and anatomical study. Reg Anesth Pain Med. 2008;33(4):369-376.

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266  Peripheral Nerve Blocks 13. Capdevila X, Pirat P, Bringuier S, et al. Continuous peripheral nerve blocks in hospital wards after orthopedic surgery: A multicenter prospective analysis of the quality of postoperative analgesia and complications in 1,416 patients. Anesthesiology. 2005;103:1035-1045. 14. Auroy Y, Benhamou D, Bargues L, et al. Major complications of regional anesthesia in France: The SOS regional anesthesia hotline service. Anesthesiology. 2002;97:1274-1280. 15. Compère V, Rey N, Baert O, et al. Major complications after 400 continuous popliteal sciatic nerve blocks for post-operative analgesia. Acta Anaesthesiol Scand. 2009;53:339-345. 16. Borgeat A, Blumenthal S, Lambert M, et al. The feasibility and complications of the continuous popliteal nerve block: A 1001-case survey. Anesth Analg. 2006;103:229-233. 17. Neuburger M, Buttner J, Blumenthal S, et al. Inflammation and infection complications of 2285 perineural catheters: A prospective study. Acta Anaesthesiol Scand. 2007;51:108-114.

18. O’Grady NP, Alexander M, Dellinger EP, et al. Guidelines for the prevention of intravascular catheter-related infections. Infect Control Hosp Epidemiol. 2002;23:759-769. 19. Vloka JD, Hadzić A. Block of the Sciatic Nerve in the Popliteal Fossa. In: Hadzić A, ed. The New York School of Regional Anesthesia Textbook of Regional Anesthesia and Acute Pain Management. New York: McGraw Hill; 2007:532-553. 20. Gaertner G, Fouche E, Chouquet, et al. Sciatic nerve block. In: Hadzić A, ed. The New York School of Regional Anesthesia Textbook of Regional Anesthesia and Acute Pain Management. New York: McGraw Hill; 2007:517-531.

Lower Extremity: Saphenous Nerve Block

27

Yi Zhang, MD, PhD, MSc Saphenous nerve entrapment or neuropathy is a relatively rare clinical entity, a paucity of data exists regarding its natural history and treatment outcome, although there are a few case reports in the literature. Saphenous nerve neuropathy is an important consideration in the differential diagnosis of lumbar radiculopathy, medial knee pain, and lower extremity vascular insufficiency. Saphenous nerve block can be an effective treatment for saphenous neuropathy or pain in the distribution of the saphenous nerve for this condition.

Anatomy of the Saphenous Nerve The saphenous nerve is the largest cutaneous branch of the femoral nerve. Sensory fibers from L3 and L4 levels contribute to this pure sensory nerve.1,2 The saphenous nerve branches off the posterior division of the femoral nerve and descends anteroinferiorly through the femoral triangle, lateral to the femoral sheath, anterior to the femoral artery and posterior to the aponeurotic covering of the adductor canal (also known as Hunter canal, subsartorial canal).1,2 It then exits from the adductor canal, descends under the sartorius muscle, and then courses around the posterior edge of the sartorius muscle at its tendon portion. In the medial aspect of the knee, the saphenous nerve descends vertically behind the sartorius muscle, pierces the fascia lata and becomes subcutaneous.1,2 At this level, the infrapatellar branch pierces the sartorius muscle and courses inferiorly to the infrapatellar region and innervates the skin in front of the patella. The infrapatellar branch communicates with the anterior cutaneous branches of the femoral nerve above the knee, and with other branches of saphenous nerve below the knee, as well as branches of the lateral femoral cutaneous nerve on the lateral side of the knee, forming the plexus patellae.1 The remaining course of the saphenous nerve then passes down along the medial aspect of the tibia, accompanied by the great saphenous vein and, divides into two branches at the lower third of the leg.1 One of the branches of the descending portion of the saphenous nerve courses along the medial border of the tibia and ends at the ankle, whereas the other branch passes anteriorly to the ankle and is distributed to the medial aspect of the foot, reaching as far as the metatarsophalangeal joint of the great toe and communicating with the medial branch of the superficial peroneal nerve (Fig. 27-1).1 The saphenous nerve supplies sensory innervations to the anterior medial aspect of the leg, including the medial malleolus (Fig. 27-2).1,2 The adductor canal, the entrapment site for the saphenous nerve, is located approximately 10 centimeters proximal to the

medial femoral condyle. It is an aponeurotic tunnel in the middle third of the thigh, extending from the apex of the femoral triangle to the opening in the adductor magnus. It courses between the anterior compartment of the thigh and the medial compartment of the thigh. The vastus medialis muscle lies anteriorly and laterally, whereas the adductor longus lies posteriorly. The content in the canal includes the femoral artery, femoral vein, and branches of the femoral nerve, the saphenous nerve, and the nerve to the vastus medialis muscle). It is covered by a strong aponeurosis that extends from the vastus medialis, across the femoral vessels to the adductor longus and magnus. The sartorius muscle lies on the aponeurosis.2 The adductor canal can be located by palpating along the anteromedial aspect of the vastus medialis muscle and then sliding posteriorly until the edge of the sartorius muscle is felt. The adductor canal is located directly beneath this point.2,3

Pathophysiology of Saphenous Nerve Entrapment and Symptoms The saphenous nerve can become entrapped in multiple locations along its long descending course from the thigh to the leg. Common sites of entrapment include the site where the nerve penetrates the roof of the adductor canal, or at the infrapatellar branch during knee surgery or varicose vein stripping surgery. Compression of the saphenous nerve against the medial femoral condyle may be caused by stirrups during lithotomy position for surgery. The pathophysiology of saphenous nerve neuropathy involves two different mechanisms: acute compression with high pressure and chronic intermittent compression by contraction and relaxation of the fibrous tissue that impinges the nerve. Demyelination of the involved nerve seems to be a common pathologic finding.3,4 Saphenous nerve entrapment typically manifests as burning pain after prolonged walking or standing in the medial knee and leg. Pain may also be present at rest. Stair climbing may aggravate pain. Sensory symptoms typically involve paresthesia, hypoesthesia, with variations due to the length of nerve compression at the entrapment site. Hyperalgesia, allodynia, and numbness may also be present in the distribution of the saphenous nerve innervation area. The pain associated with this neuropathy may be referred to the lower medial aspect of the knee, or it may radiate down the medial aspect of the lower extremity to the ankle and foot.3,4 There is no motor compromise because the saphenous nerve is a purely sensory nerve. This is important in differentiating this syndrome from radiculopathy in the L4 dermatome distribution. 267

268  Peripheral Nerve Blocks

Sartorius Lateral femoral cutaneous

Iliacus Femoral Psoas major Lumboinguinal L.1.2. Pectineus

Anterior cutaneous

Rectus femoris Vastus lateralis

Adductor longus

Lateral femoral cutaneous L.2.3.

Ilioinguinal L.1.2.

Anterior division of obturator Medial branch of anterior cutaneous

Anterior femoral cutaneous L. 2. 3.

Gracilis Saphenous

Vastus medialis

Common peroneal L. 0. S. 1. 2.

Extensor digitorum longus Superficial peroneal Deep peroneal

Saphenous L.S.4. Superficial peroneal L.4.5.8.1.

Sural S.1.2.

Deep peroneal L.1.5.

Figure 27-2  Saphenous nerve innervation area. (From Williams PL, Warwick R: Gray’s Anatomy, 36th ed. Philadelphia, WB Saunders; 1980.)

of the sensory nerve action potential (SNAP) can be seen. However, in some cases SNAP of the saphenous nerve may be difficult to record, even in the unaffected leg. In this event, cortical sensory evoked potential recording may be used to help diagnose this condition.5 Figure 27-1  Anatomy of saphenous nerve. (From Williams PL, Warwick R: Gray’s Anatomy, 36th ed. Philadelphia, WB Saunders; 1980.)

Clinical criteria for the diagnosis of saphenous nerve entrapment neuropathy include pain in the distribution of the saphenous nerve, normal motor function, and tenderness to palpation over the entrapment site. Entrapment site tenderness is a key feature of saphenous nerve neuropathy. Vigorous palpation at the exit point for the saphenous nerve may result in local pain and referred pain in the nerve’s distribution.3,4 Electrodiagnostic studies are a valuable tool in diagnosing saphenous nerve entrapment. Changes in latency and amplitude

Indications for Saphenous Nerve Block Entrapment in the adductor canal is usually treated conservatively. Avoiding aggravating activities and using proper body mechanics will also be helpful. Transcutaneous electrical nerve stimulation (TENS) unit may also be effective in pain control relief. Saphenous nerve block (with or without corticosteroid) is frequently used for saphenous nerve entrapment neuropathy. This injection may need to be repeated periodically. Contraindications for saphenous nerve block of this procedure include overlying infection, severe bleeding disorder or coagulopathy and preexisting neurologic damage in the affected area.

Lower Extremity: Saphenous Nerve Block  269

Technique Block of saphenous nerve for entrapment neuropathy is often performed at the adductor canal because this is often the site of entrapment. A transsartorial approach is most frequently used.6 The patient lies in the supine position, the sartorius muscle is palpated just above the knee with the leg extended and actively elevated. A skin wheal is raised over the sartorius muscle belly. The needle is inserted at 1-finger width above the patella slightly posterior to the coronal plane and slightly caudal, through the muscle belly of the sartorius until a loss of resistance identifies the subsartorial adipose tissue. The depth of insertion is typically between 1.5 and 3 cm.7 After negative aspiration for blood, 5 mL of local anesthetics (lidocaine or bupivacaine) and 20 to 40 mg of triamcinolone is injected. The saphenous nerve can also be located by eliciting paresthesia in the distribution of the nerve.8 In this approach, the patient is placed in the lateral position with the leg slightly flexed. The medial condyle of the femur is palpated. A point just in front of the posterior edge of the medial condyle is then identified and prepped. A 1⁄2 inch, 25-gauge needle in then advanced through this point toward the medial condyle of the femur until a paresthesia in the distribution of the saphenous nerve is elicited (Figs. 27-3 and 27-4). When a paresthesia in the distribution of the saphenous nerve is elicited, the needle is withdrawn 1 mm and the patient is observed to be sure that there is no persistent paresthesia. The mix of local anesthetics and corticosteroid can then be injected.8 Ultrasound-guided saphenous nerve block technique has been adopted in recent years.9-11 In this approach, the patient is placed supine with the leg slightly externally rotated. Using a linear transducer with the appropriate frequency range (10 to 12 MHz), the distal one third of the thigh is scanned distally toward the knee. In the distal thigh, the saphenous nerve is predominantly hyperechoic and located posterior to the sartorius muscle in the subsartorial compartment (Fig. 27-5). The vastus medialis muscle lies medially to the sartorius muscle. The transducer is

placed over the medial aspect of the right distal thigh transverse to the course of the saphenous nerve. A 5 to 8 cm 22-gauge needle is inserted and advanced in parallel to the transducer and the ultrasound beam in the lateral to medial direction until it reaches the fascial plane between the sartorius and vastus medialis muscles. After negative aspiration, the mix of local anesthetics and corticosteroid can then be injected.9-11

Complications Saphenous nerve block is a relatively simple procedure with few complications. Incidence of hematoma from vascular injury can be minimized by avoiding multiple needle insertions and avoiding

Saphenous nerve

Figure 27-4  Saphenous nerve block at the femoral medial condyle. (From Waldman S. Atlas of Interventional Pain Management. 2nd ed. Philadelphia: WB Saunders; 2003.)

Anterior

Vastus medialis muscle Saphenous nerve SM

SN

Sartorius muscle Medial Figure 27-3  Saphenous nerve block at knee at the subsartorial space. (From Brown DL. Atlas of Regional Anesthesia, 2nd ed. Philadelphia: WB Saunders; 1999.)

Femur Figure 27-5  Ultrasound appearance of the saphenous nerve. At the distal thigh, the saphenous nerve lies underneath the sartorius muscle. (From Marhofer P. Ultrasound Guidance for Nerve Blocks: Principle and Practical Implementation. Cambridge: Oxford University Press; 2008.)

27

270  Peripheral Nerve Blocks

insertion of the needle through superficial veins. Nerve injury, can be minimized by avoiding injection if high pressures are felt on injection or if patient reports paresthesia or pain in the distribution of the nerve on injection, suggesting intraneural placement of the needle tip.

Other Treatments Avoiding aggravating activities and using proper body mechanics will also be helpful in alleviating pain symptoms. Use of a TENS unit may also be effective in pain control. If repeated saphenous nerve blocks fail to relieve pain, surgical decompression may be considered.

Conclusion Saphenous nerve entrapment or neuropathy is a relatively rare clinical entity, causing pain in the lower medial aspect of the knee, and it may radiate down the medial aspect of the lower extremity to the ankle and foot, without motor compromise. Saphenous nerve block can be an effective treatment for saphenous neuropathy or pain in the distribution of the saphenous nerve.

REFERENCES   1. Williams PL, Warwick R. Gray’s Anatomy. 36th ed. Philadelphia: WB Saunders; 1980.   2. Sauerland EK, Patrick W, Tank PW. Grant’s Dissector. Hagerstown, Md: Lippincott Williams & Wilkins; 2005.   3. Romanoff ME, Cory PC, Kalenak A, et al. Saphenous nerve entrapment at the adductor canal. Am J Sports Med. 1989;17:478-481.   4. Worth RM, Kettelkamp DB, Defalque RJ, Duane KU. Saphenous nerve entrapment—A cause of medial knee pain. Am J Sports Med. 1984;12:80-81.   5. Tranier S, Durey A, Chevallier B, Liot F. Value of somatosensory evoked potentials in saphenous entrapment neuropathy. J Neurol Neurosurg Psychiatry. 1992;55:461-465.   6. van der Wal M, Lang SA, Yip RW. Transsartorial approach for saphenous nerve block. Can J Anaesth. 1993;40(6):542-546.   7. Brown DL. Atlas of regional anesthesia. 2nd ed. Philadelphia: WB Saunders; 1999.   8. Waldman S. Atlas of Interventional Pain Management. 2nd ed. Philadelphia: WB Saunders; 2003.   9. Lundblad M, Kapral S, Marhofer P, Lönnqvist PA. Ultrasound-guided infrapatellar nerve block in human volunteers: Description of a novel technique. Br J Anaesth. 2006;97:710-714. 10. Krombach J, Gray AT. Sonography for saphenous nerve block near the adductor canal. Reg Anesth Pain Med. 2007;32:369-370. 11. Marhofer P. Ultrasound Guidance for Nerve Blocks: Principle and Practical Implementation. Oxford University Press; 2008.

Lower Extremity: Lateral ­Femoral Cutaneous Nerve Block

28

Shihab Ahmed, MD, MPH

The clinical description of pain, numbness, and tingling involving the anterior and lateral thigh, was first described by Bernhardt in 1878.1 Werner Hager (1885) was the first to describe compression of the lateral femoral cutaneous nerve near the anterior superior iliac spine (ASIS) as the cause of pain near the hip.2 In 1895, both Bernhardt and Roth published separate articles on meralgia paresthetica (MP).3,4 Roth described five patients with similar symptoms and coined the term “meralgia paresthetica” from the Greek words meros for thigh and algos meaning pain.4

Anatomy of the Lateral Femoral Cutaneous Nerve The lateral femoral cutaneous nerve (LFCN) is derived from the lumbar plexus and its contribution comes mostly from the L2 and L3 nerve roots.5 The LFCN may derive from various other combinations such as L2 and L3, L1 and L2, or L2 or L3 alone.6 The LFCN appears at the lateral border of the psoas muscle just above the crest of the ilium.5 The nerve then travels laterally and inferiorly across the surface of the iliacus muscle from which it is separated by a thin muscle sheath (Fig. 28-1). Both the nerve and the iliacus muscle are covered with a dense fascial layer called the iliac fascia, which is composed of two layers and the LFCN travels between them.7 The nerve continues its course toward the lateral portion of the inguinal ligament posterior to the deep circumflex iliac artery, which courses parallel to the inguinal ligament beneath the iliac fascia.7 Filho and coworkers found in their cadaver study that the anterior lamina of the iliac fascia and the transversalis fasciae fused to form the iliopubic tract (IPT) and the LFCN courses deep to the IPT and reaches the thigh by passing posterior to the inguinal ligament (IL).7 There are several descriptions of anatomic variations of LFCN as it travels from the pelvis to the thigh based on cadaver studies and surgical exploration of the LFCN for meralgia paresthetica.7-12 Keegan and colleagues describes the LFCN as traveling between the two slips of lateral attachment of the IL to the anterior superior iliac spine (ASIS) and remaining just inferior and medial to ASIS.5 It then continues its course anterior to the tendinous origin and upper fibers of the sartorius muscle, separated only by the muscle sheath and covered with the fascia lata. Carai and associates reviewed descriptions of surgical explorations of the LFCN for the treatment of MP and found that in 85.2% of cases the nerve leaves the pelvis beneath the IL (Fig. 28-2).8 This pattern was also documented by Filho and coworkers in their cadaver study where all LFCNs passed posterior to the IL.7 This study also found that in

94% of cases the nerve passed 3.0 cm or less medial to the ASIS.7 Similar results were also described by Grothaus and associates in their cadaver study, in which all the nerves leave under the IL and approximately 36 mm medial to the ASIS.9 Interestingly, they also found that the nerve divides 27.6% of the time before crossing the IL, which may have important implications for nerve blocks or surgical treatment of MP. Aszmann and colleagues in their cadaver study found five variations of the LFCNs as they enter from pelvis to thigh (Fig. 28-3). In 52 cadavers, they found that the nerve overlies the iliac crest 4% (type A), ensheathed by the IL 27% (type B), ensheathed by the tendinous origin of the sartorius muscle 23% (type C), deep to the IL and medial to the sartorius muscle 26% (type D), and 20% of the time the nerve lies medial and on top of the iliopsoas muscle (type E).10 After emerging from the pelvis, the LFCN passes anterior to the tendinous attachment and upper fibers of the sartorius muscle, separated by the muscle sheath and covered by the thick fascia lata.5 Others, however, describe that the nerve may pass over, under, or through the proximal portion of the sartorius muscle.7 Filho and coworkers describes three basic patterns of terminal branching of the LFCN in 26 cadavers.7 The most common pattern (54%) is the bifurcation into anterior and poster­ ior branches (Fig. 28-4). The anterior branch again divides into medial and lateral branches and supplies the anterolateral thigh and the posterior branch supplies the proximal part of the lateral thigh. In a significant number of cases (34%), the nerve divides into medial and lateral branches and supplies the medial and lateral portion of the anterolateral thigh. In 12% of cases, the nerve trifurcates instead of bifurcating. They also observed, in most cases, that the terminal branches, rather than the trunk, pierce the fascia lata to enter the subcutaneous tissues.

Etiology Meralgia paresthetica is a peripheral sensory mononeuropathy of the LFCN. The etiology of MP can be divided into two major categories—spontaneous and iatrogenic (Fig. 28-5). Spontaneous causes include mechanical compression of the nerve or metabolic derangements in the absence of prior surgical procedures that may have injured the nerve. Other mechanical factors include obesity, pregnancy, ascites,12 pelvic tumor,13 tumor in the iliac crest,14 tight trousers,15 corsets, tight belts with accompanying holster for a pistol,16 and soldiers wearing body armor.17 MP has also been described in limb-length discrepancy18 and following the treatment of osteoid sarcoma in children.19 271

272  Peripheral Nerve Blocks

LFCN

Front

Down Figure 28-2  Emergence of the nerve from the pelvis under the inguinal ligament. (Adapted from Carai A, Fenu G, Sechi E, et al: Anatomic variability of the lateral femoral cutaneous nerve: Findings from a surgical series. Clin Anat. 2009;22:365-370.) Figure 28-1  The anatomic course of the lateral femoral cutaneous nerve (LFCN). (Adapted from Mirovsky Y, Neuwirth M: Injuries to the lateral femo­ ral cutaneous nerve during spine surgery. Spine. 2000;25:1266-1269.)

The iatrogenic causes of MP are described after various surgical procedures. This may be caused by direct trauma to the nerve during the procedure, related to patient positioning for the surgery,20 or related to postsurgical scarring.21 The surgical procedures may be classified as orthopedic and nonorthopedic procedures. The orthopedic procedures include pelvic osteotomy,22 acetabular fracture surgery,23 and bone-graft harvesting from the iliac crest.21,24,25 The nonorthopedic surgeries that have been associated with MP are laparoscopic hernia repair,26 laparoscopic cholecystectomy,27 and bariatric surgery.28

Pathophysiology A key factor in the pathogenesis of MP is likely the significant anatomic variation of the nerve described in various cadavers and surgical studies.7-10 Filho and his colleagues,7 in a cadaver study, described the pelvic portion of the LFCN and its relationship with iliac fascia and other muscles and fascia of the anterior abdominal wall. They illustrate that the anterior lamina of the iliac fascia (ALIF) fuses with the transversalis fascia to form the iliopubic tract (IPT) and continues further to meet with the IL. In their study all LFCNs passed inferior to the IPT and were in contact with it (Fig. 28-6). The angle between the ALIF and the IPT becomes more obtuse as the lower abdominal wall moves anteriorly and inferiorly as occurs in obesity (see Fig. 28-4). The authors hypothesized that because the ALIF is firmly attached with the muscles of the abdominal wall, with obesity the ALIF is pushed inferiorly to compress the LFCN. The authors speculated that with erect posture, gravity may further exacerbate the situation by pulling the adipose tissue and the viscera, reflecting the worsening symptoms of patients of MP seen with standing and improving on lying down. Based on their findings of the widening of the LFCN just proximal to the IL, the authors speculate that the nerve may also be compressed within the “LFCN tunnel”

(beginning under the IPT and finishing at the IL). It has been found that the groin pressure was greater in sitting obese patients than in subjects with normal weight.29 This becomes more important when the nerve course is close to the ASIS (types A, B, and C, see Fig. 28-3).10 This may increase the likelihood of nerve compression, especially in obese individuals and those with hip extension.10,11 Many researchers suggest that the usual traumatic site for the LFCN is at the IL.5,9,30,31 Keegan and coworkers describe the emergence of the LFCN between the two slips of the lateral attachment that may be affected by the tension of the ligament.5 The authors’ point to the attachment of muscles and fascia and the role they may play with the tension of the ligament. The sartorius muscle has a medial aponeurotic expansion that attaches to the inferior border of the IL and may cause episodic depression of the ligament with muscle contraction. The IL also provides an insertion for the external oblique muscle and an origin for the lowest fibers of the internal oblique and transversus abdominis muscles and thereby create tension by the contraction of these muscles. The deep layer of the superficial abdominal fascia, or Scarpa fascia, extends downward one half inch below the IL to attach with the fascia lata. This attachment with the fascia lata may cause a downward pull of the IL among patients with dependent abdominal fat.5

Diagnosis Diagnosis of MP is usually done by history and physical examination, with the characteristic location of pain and numbness confined to the anterolateral thigh (Fig. 28-7).32 In rare cases, the area may extend inferiorly below the knee, gluteal region, and medial thigh.12,32 The patient describes their symptoms as burning, coldness, lightning pain, deep muscle achiness, tingling or crawling sensations, and frank anesthesia. Walking, standing, or getting in and out of automobiles usually provokes symptoms. Sitting may relieve symptoms in some patients but exacerbate the symptoms in others. Dureja and associates describe their diagnostic criteria

Lower Extremity: Lateral Femoral Cutaneous Nerve Block  273

28

Type A

Type B

Type D

Type C

Type E

based on a series of 40 patients treated for MP. They describe their clinical criteria for the diagnosis: (1) unpleasant paresthesias/numbness/burning sensation/dysesthesias/pain over the anterolateral aspect of the thigh and exacerbation of symptoms on walking, standing, or extending the hip.33 They found unpleasant paresthesias over the anterolateral aspect of the thigh is the most frequent symptom (85%). Tingling or throbbing pain in the thigh was reported by 75% of patients and 25% complained of hypersensitivity in the form of discomfort from the clothing over the painful area. Physical examination may find an area of hair loss on the anterolateral thigh due to the patient’s rubbing of the thigh. Sensory examination may reveal hypesthesia, dysesthesia, with or without mechanical allodynia. Hip extension and standing in erect posture



Figure 28-3  Five common variant locations of the LFCN as it exits the pelvis of 52 cadavers (see text for details). (Adapted   from Aszmann OC, Dellon ES, Dellon AL: Anatomical course of the lateral femoral cutaneous nerve and its susceptibility to   compression and injury. Plast Reconstr Surg. 1997;100:600-604.)

can elicit concordant pain. Focal tapping near the ASIS (Tinel sign) may reproduce the usual pain in certain cases. A pelvic compression test has recently been described to assist the diagnosis of MP (Fig. 28-8).34 The idea is that the LFCN is compressed by the IL and relaxing the ligament should relieve the pressure on the nerve and thereby alleviate the pain. The patient is placed in the lateral decubitus position with the affected side up and is asked to focus on their symptoms while the examiner applies the lateral compression on the pelvis for 45 seconds. The test is considered positive if patient’s symptoms improve. When compared with the electrophysiologic diagnosis, the authors found the sensitivity and specificity of the test 95% and 93%, respectively. Electrodiagnostic studies can be a helpful adjunct to confirm the diagnosis of MP. Sensory nerve conduction velocity (SNCV)

274  Peripheral Nerve Blocks

of the LFCN and somatosensory evoked potentials (SSEP) recorded on the scalp following stimulation of the trunk of the LFCN or by stimulating the skin innervated by the LFCN are the most common electrodiagnostic tests for MP. Seror compared the SNCV and the SSEP in 30 patients with clinical evidence of unilateral MP and concluded that SNCV is more accurate in diagnosing MP.35 In a later study, the same author found that SSEP may be beneficial in obese patients where SNCV cannot be measured.36 A differential diagnosis of MP includes upper lumbar nerve root irritation, although this is not common. Neurologic abnormality in MP is always sensory dysfunction; there should not be any motor or reflex abnormality and a straight leg raising test and sciatic notch tenderness will be absent. Electrodiagnostic tests and magnetic resonance imaging will help to differentiate MP from lumbar radiculopathy. If the presentation includes any gastrointestinal Lateral femoral cutaneous nerve ASIS Inguinal ligament 5 cm

Sartorius muscle Anterior Posterior

Figure 28-4  Lateral femoral cutaneous nerve divides into anterior and posterior divisions on the surface of the sartorius muscle approximately 5 cm below the anterior superior iliac spine (ASIS) in most patients in this study. (Adapted from Grothaus CM, Holt M, et al: Lateral femoral cutaneous nerve: An anatomic study. Clin Orthop Relat Res. 2005;437:164-168.)

and urogenital symptoms, pelvic etiology should be considered and an abdominal/pelvic ultrasound and or computerized tomography should be performed for further evaluation.

Treatment Most patients with MP improve with conservative treatment.12,33,37,38 Conservative therapies applied in various series are different and therefore it is difficult to make any comparisons regarding the efficacy of one modality versus another. Conservative therapy begins with removal of any inciting agents such as tight belts, braces, casts, tight trousers (taille basse), tight undergarments, and various duty uniform belts used by police offices and carpenters. Initial measures also include local application of ice packs and oral antiinflammatory agents to reduce local inflammation. Other established neuropathic agents such as tricyclic antidepressants, anticonvulsants, antiarrhythmics39 can also be considered as an adjunct therapy for MP. Application of a topical anesthetic patch has been used for neuropathic pain and may be considered as part of the conservative treatment for MP.40 If symptoms persist, LFCN block with local anesthetics and steroid should be considered.33,38 Repeat injections of local anesthetics and steroid may be needed to achieve persistent relief.33,38 In their series, Dureja and his colleagues performed a diagnostic LFCN block with 8 mL of 0.25% bupivacaine in forty patients. If the patient responded, nerve blocks were repeated on alternate days with bupivacaine and methylprednisolone, 20 mg each up to a total dose of 80 to 120 mg, a minimum of five blocks in each patient.33 The patients also received oral diphen­ylhydantoin in a dose range of 100 to 300 mg daily in divided doses for 10 to 12 weeks. Thirty four (85%) had complete relief of paresthesias within 10 weeks. Surgical therapy is reserved for refractory and intractable symptoms in patients with MP. Fortunately, only a small portion of the patients with the diagnosis of MP require surgical interventions. Surgical intervention to relieve the symptoms of MP dates back to 1885.12 The surgery for MP can be divided into neurolysis of the tissue constricting the nerve, neurolysis and transposition of the LFCN, and transection with excision of a portion of the nerve. Which of these three treatments is superior remains unsettled. Among the previous series, the success rate from

Etiology

Iatrogenic

Spontaneous

Mechanical

Metabolic

Orthopedic surgeries

Nonorthopedic surgeries

Obesity, pregnancy, corsets, tight trousers, etc.

Diabetes, alcoholism, and lead poisoning

Spine surgeries, pelvic osteotomy, iliac crest bone graft, hip replacement, etc.

Laparoscopic inguinal hernia repair

Figure 28-5  Algorithm for etiology.

Lower Extremity: Lateral Femoral Cutaneous Nerve Block  275

long-term follow-up. The author recommends that adults with symptoms of less than 1 year and all pediatric patients should undergo ­neurolysis. If symptoms persist after the surgery, resection should be considered. He also suggests primary resection for adults with more than a 1-year history of refractory pain. During surgical intervention, a suprainguinal or infrainguinal approach is taken to explore the nerve for decompression or transection. The infrainguinal approach is made 3 cm below and parallel to the IL down to the fascia lata, which is then incised in the same direction.47 The nerve is then exposed medial to the sartorius muscle and followed proximally toward the IL. For the suprainguinal approach, an incision is made 1 cm above and parallel to the IL.48 The suprainguinal approach allows for accurate identification of the LFCN in its intrapelvic and retroperitoneal location and is followed distally toward the IL.

neurolysis of the LFCN for refractory MP varies from 60% to 90%.41-43 However, in a more recent case series Siu and ­colleagues found complete and partial symptom relief in 73% and 20% cases, respectively, from neurolysis with an average follow-up of 4.1  years.44 Williams and Trzil reported successful relief of symptoms of 23 out of 24 patients after LFCN transection.12 Although the surgery did cause permanent anesthesia in the ­anterolateral thigh, there were no other serious complications from the ­surgery. In another series of 21 patients, van Eerten concluded that to accomplish complete pain relief, transection of the nerve is superior to neurolysis for refractory MP.45 Ivins described neurolysis in four of eight operative cases of MP.46 All four had immediate relief, but symptoms returned 2 to 24 months later. All four underwent resection and had no recurrence. The other four had primary transection and had persistent relief at 67

4

9

3 1

10

2

15 15

A

A

Figure 28-6  Parasagittal diagrams near the anterior superior iliac spine. A, Flat abdomen. 1, lateral femoral cutaneous nerve; 2, iliopubic tract; 3, transversalis fascia; 4, subserous tissue; 5, parietal peritoneum; 6, transver­ sus abdominis muscle; 7, internal oblique muscle; 8, skin; 9, subcutaneous tissue; 10, aponeurosis of external oblique muscle; 11, inguinal ligament; 12, fascia lata; 13, iliacus muscle; 14, head of femur; 15, laminae of iliac fascia. B, Distended abdomen. Black arrows indicate the traction downward due to abdominal distention   (in ascites, pregnancy, etc.), the weight of the viscera or the burden that results from abundant subcutaneous adipose tissue. White arrows indicate the critical area of nerve compression. (Adapted from Filho LCD, Valenca MM, Guimaraes Filho FAV, et al: Lateral   femoral cutaneous neuralgia: An anatomical insight.   Clin Anat. 2003;16:309-316.)

8

5

11

14

B

13 12

B

C

Figure 28-7  Area of numbness and dysesthesia among the patients with MP. Solid lines (A-C) represent area of dysesthesia; broken lines represent area of additional pain. (From Ivins GK: Meralgia paresthetica, the elusive diagnosis: Clinical experience with 14 adult patients. Ann Surg. 2000;232:281-286.)

28

276  Peripheral Nerve Blocks

A

and nerve stimulator-assisted block and the patient group had only nerve stimulator-guided block. The authors began the nerve stimulator-assisted block by identifying the likely location of the nerve below the IL by a hand-held transdermal nerve stimulator. The location of the nerve stimulator from where the maximum paresthesia over the lateral thigh was felt was marked. A 26-gauge uninsulated needle was attached to a nerve stimulator (pulse width 100 to 200 μsec: 1 Hz) and inserted at the same location to localize the nerve further. A paresthesia over the lateral thigh at 0.6 mA was considered adequate. To block the nerve, 6 mL of 2% lidocaine with 1:200,000 epinephrine was injected. The authors found the nerve stimulator-assisted technique was successful in all volunteers (100%) and 85% of the patients. They found the success rate was only 40% with the classic fan technique among the volunteers.

Ultrasound-Guided Nerve Block

B Figure 28-8  The pelvic compression test (see text for details). (Adapted from Nouraei SA, Anand B, Spink G, O’Neill KS: A novel approach to the   diagnosis and management of meralgia paresthetica. Neurosurgery. 2007;  60:696-700.)

LFCN Nerve Block The LFCN block has been described for both acute and chronic pain conditions such as MP. Examples of acute pain conditions include anesthesia and analgesia for immediate postoperative situations such as knee arthroscopy,49 vastus lateralis muscle biopsy to detect malignant hyperthermia,50 and skin grafting.51

Classic Block Technique52 The patient is placed in a supine position and appropriately undressed to identify the topographic landmarks. The ASIS is palpated and its location is marked with a skin marker. The location of the IL can be visualized as a shallow line or by drawing a line by connecting the ASIS and the pubic tubercle. The target point for the needle insertion is 2 to 3 cm medial and 2 to 3 cm inferior from the ASIS. A skin wheal is made with local anesthetic at the needle insertion site. A short bevel 22-gauge, 4-cm needle with syringe attached is inserted perpendicular to the skin entry site. The needle is advanced until a sudden release indicating passage through the fascia lata occurs. After negative aspiration, approximately two thirds of a total 10 mL volume of local anesthetic solution is deposited under the fascia lata and the rest is injected above it. The local anesthetic solution is deposited in a fan-like manner with the needle moving laterally and medially. Any sudden sharp or radiating pain may indicate perineural injection of local anesthetics and should be avoided. The risk of intravascular injection of local anesthetics during the nerve block is unlikely because of the medial location of the femoral vessels.

Block with Nerve Stimulator53 Shannon and colleagues described the technique of LFCN block using a nerve stimulator. Their study consisted of patients and healthy volunteers. The volunteer group had classic fan technique

Peripheral nerve block with ultrasound guidance allows visualizing the surrounding anatomy and placement of the needle at the target location in real time. When compared with conventional techniques, ultrasound-guided nerve blocks have been found to be superior during brachial plexus, ilioinguinal, and iliohypogastric nerve blocks.54,55 The accuracy of the ultrasound probe to identify the LFCN has now been documented.56,57 Among 19 cadavers, using the ultrasound probe, Ng and associates was able to place the needle in contact with the nerve in 16 cases and in the rest, the three-needle tips were 2, 3, and 12 mm away from the nerve trunk.58 Contrary to traditional techniques (2 to 3 cm medial and inferior to the ASIS), only one of the 19 needles was in contact with the nerve. In the same study, the authors also compared the placement of the nerve stimulation needle via ultrasound guidance or using the aforementioned landmark. They were able to identify all twenty LFCNs via ultrasound and the nerve was clearly visualized between the two fascial layers. In 16 of 20 patients, the nerve was identified by the ultrasound corresponding to the nerve position identified by the nerve stimulation. However, none of the skin-marked locations based on anatomic landmarks corresponded to the actual position of the LFCN identified by the nerve stimulation technique. The authors described that the best view of the LFCN was obtained by transverse scanning at 14.1 mm medial and 50.8 mm inferior to the ASIS. A high-frequency (>7 MHz) linear array transducer is recommended for identification of the nerve. The successful nerve block has been reported using needles with and without stimulating capability.56,57 The technique requires that the patient is lying supine with a wide sterile preparation around the groin and upper thigh. The ASIS is identified and marked with a sterile skin marker. The ultrasound probe scans transversely with the lateral end of the probe just inferior to the ASIS to identify the sartorius muscle (Fig. 28-9). The probe is then slid slowly medially and inferiorly below the IL to identify the two continuous hyperechoic lines under the subcutaneous tissue, the fascia lata, and fascia iliaca. The LFCN will appear in cross-section in the space between the two fascial layers. It will appear as an oval hyperechoic structure containing several circular hypoechoic dots giving it a “honeycomb” appearance (Fig. 28-10). After identifying the nerve, its course is then traced by scanning the structure proximally and distally. The operator should also scan medially to verify the neurovascular bundle of the femoral nerve, artery, and vein. If the nerve is not identified by this technique, one should consider the possible anatomic variations as discussed earlier. The operator may expand the area and scan more medial and lateral to the ASIS.

Lower Extremity: Lateral Femoral Cutaneous Nerve Block  277

28

Cephalad ASIS

IL Lateral

e

edl

Ne

FL FL N Sart. m.

A Lateral

Medial

FL N

Caudad

LA Sart. m.

Figure 28-9  The ultrasound probe placed on the skin in a transverse plane immediately inferior to the anterior superior iliac spine (ASIS). (From Ng I, Vaghadia H, Choi PT: Ultrasound imaging accurately identifies the lateral femoral cutaneous nerve. Anesth Analg. 2008;107:1070-1074.) 0+

FL

Lateral

B

T Lel LFC

Figure 28-11  A, Ultrasonographic view of lateral femoral cutaneous nerve (LFCN) before injection. B, Ultrasonographic view of LFCN after injection. FI, fascia iliaca; FL, fascia lata; LA, local anesthetic and steroid spreading around LFCN; LFCN, lateral femoral cutaneous nerve; N, LFCN; Sart. m., sartorius muscle. (From Tumber PS, Bhatia A, Chan VW: Ultrasound-guided lateral femoral cutaneous nerve block for meralgia paresthetica. Anesth Analg. 2008;106:1021-1022.)

anterolateral thigh. When confirmed, injection of local anesthetics with or without corticosteroid is carried out after negative aspiration. The perineural spread is visualized on the ultrasound screen (Fig. 28-11). Although the range of total volume of injectate varies, with ultrasound-guided localization of the nerve, a successful block has been achieved using as little as 1 mL of injectate.57

Complications and Contraindications to Block Figure 28-10  Ultrasound image of the lateral femoral cutaneous nerve (LFCN) in the short axis. The honeycomb texture of the nerve in this view can be visualized and is bordered by arrows.57 (From Hurdle MF, Weingarten TN, Crisostomo RA, et al: Ultrasound-guided blockade of the lateral femoral cutaneous nerve: Technical description and review of 10 cases. Arch Phys Med Rehabil. 2007;88:1362-1364.)

When the LFCN is located, under strict sterile conditions, the needle is passed under direct visualization toward the LFCN. The needle is advanced keeping it in a longitudinal plane to ensure  the visualization of the entire needle. If a nerve stimulator needle is used, stimulation will cause paresthesia over the

Complications with LFCN block are rare, but can include nerve injury, vascular injury, peritoneal entry, seizures from local anesthetic, and infection. Contraindications to block include coagulopathy, ongoing infection, allergy to local anesthetics or corticosteroids, or patient refusal.

Conclusion Meralgia paresthetica is a peripheral sensory neuropathy of the lateral femoral cutaneous nerve. The etiology of MP may be postsurgical, mechanical, or metabolic. A key issue in the pathogenesis

278  Peripheral Nerve Blocks

of MP is the significant anatomic variation of the nerve during its course through pelvis and anterior thigh. Many investigators suggest that the traumatic site for the LFCN is near the inguinal ligament. In most circumstances, the diagnosis of the MP is done with history and physical examination. Usually there are characteristic pain and associated numbness over the anterolateral thigh. Electrodiagnostic studies can also be helpful to confirm the diagnosis of MP. A majority of the patients with MP improve with conservative therapies starting with removal of any inciting agents such as tight belts. Initial measures also include local application of icepacks, antiinflammatory medication, and neuropathic pain medications. If symptoms persist, the LFCN block with local anesthetic and steroid is recommended. The procedure can be done following the surface landmarks near the IL. However, the use of ultrasound guidance may increase the likelihood of targeted injection. Only a few refractory MP patients are referred for possible surgical exploration. REFERENCES   1. Bernhardt M. Neuropathologische Beobachtungen. I. periphere Lahmungen. D Arch Klin Med. 1878;22:362-393.   2. Hager W. Neuralgia femoris. Resection des Nerv. Cutan. Femoris anterior externus. Heilung. Deutsch Med Wochenschr. 1885;11:218-219.   3. Bernhardt M. Ueber isolirt im Gebiete des N. Cutaneous femoris externus vorkommende Parasthesien. Neurol Centrabl. 1895;14:242-244.   4. Roth V. [Meralgia Paresthetica]. Med Obozr. 1895;43:678.   5. Keegan JJ, Holyoke EA: Meralgia paresthetica: An anatomical and surgical study. J Neurosurg.1962;19:341-345.   6. Sunderland S. Nerves and nerve injuries. Edinburgh: E & S Livingstone; 1968.   7. Filho LCD, Valenca MM, Guimaraes Filho FAV, et al. Lateral femoral cutaneous neuralgia: An anatomical insight. Clin Anat. 2003;16:309-316.   8. Carai A, Fenu G, Sechi E, et al. Anatomical variability of the lateral femoral cutaneous nerve: Findings from a surgical series. Clin Anat. 2009;22:365-370.   9. Grothaus MC, Holt M, Mekhail AO, et al. Lateral femoral cutaneous nerve: An anatomic study. Clin Orthop Relat Res. 2005;437: 164-168. 10. Aszmann OC, Dellon ES, Dellon AL. Anatomical course of the lateral femoral cutaneous nerve and its susceptibility to compression and injury. Plast Reconstr Surg. 1997;100:600-604. 11. Grossman MG, Ducey SA, Nadler SS, Levy AS. Meralgia paresthetica: Diagnosis and treatment. J Am Acad Orthop Surg. 2001;9:336-344. 12. Williams PH, Trzil KP. Management of meralgia paresthetica. J Neurosurg. 1991;74:76-80. 13. Suber DA, Massey EW. Pelvic mass presenting as meralgia paresthetica. Obstet Gynecol. 1979;53:257-258. 14. Tharion G, Bhattacharji S. Malignant secondary deposit in the iliac crest masquerading as meralgia paresthetica. Arch Phys Med Rehabil. 1997;78:1010-1011. 15. Boyce JR. Meralgia paresthetica and tight trousers. JAMA. 1984;251:1553. 16. Korkmaz N, Ozcakar L. Meralgia paresthetica in a policeman: The belt or the gun. Plast Reconstr Surg. 2004;114:1012-1013. 17. Fargo MV, Konitzer LN. Meralgis paresthetica due to body armor wear in U.S. soldiers serving in Iraq: A case report and review of the literature. Mil Med. 2007;172:663-665. 18. Goel A. Meralgia paresthetica secondary to limb length discrepancy: Case report. Arch Phys Med Rehabil. 1999;80:348-349. 19. Edelson R, Stevens P. Meralgia paresthetica in children. J Bone Joint Surg Am. 1994;76:993-999. 20. Mirovsky Y, Neuwirth M. Injuries to the lateral femoral cutaneous nerve during spine surgery. Spine. 2000;25:1266-1269. 21. Weikel AM, Habal MB. Meralgia paresthetica: A complication of iliac bone procurement. Plast Reconstr Surg. 1977;60:572-574.

22. Hogh J, Macnicol MF. The Chiari pelvic osteotomy. A long-term review of clinical and radiographic results. J Bone Joint Surg Br. 1987;69:365-373. 23. de Ridder VA, de Lange S, Popta JV. Anatomical variations of the lateral femoral cutaneous nerve and the consequences for surgery. J Orthop Trauma. 1999;13:207-211. 24. Massey EW. Meralgia paresthetica secondary to trauma of bone graft. J Trauma. 1980;20:342-343. 25. Banwart JC, Asher MA, Hassanein RS. Iliac crest bone graft harvest donor site morbidity: A statistical evaluation. Spine. 1995;20:1055-1060. 26. Dibenedetto LM, Lei Q, Gilroy AM, et al. Variations in the inferior pelvic pathway of the lateral femoral cutaneous nerve: Implications for laparoscopic hernia repair. Clin Anat. 1996;9:232-236. 27. Yamout B, Tayyim A, Farhat W. Meralgia paresthetica as a complication of laparoscopic cholecystectomy. Clin Neurol Neurosurg. 1994;96:143-144. 28. Macgregor AM, Thoburn EK. Meralgia paresthetica following bariatric surgery. Obes Surg. 1999;9:364-368. 29. Deal CL, Canoso JJ. Meralgia paresthetica and large abdomens. Ann Intern Med. 1982;96:787-788. 30. Lee FC. Meralgia paresthetica. Int Clin. 1936;1:216-229. 31. Mack EW. Meralgia paresthetica: New causal observations. West J Surg Obstet Gynecol. 1946;54:390-391. 32. Ivins GK. Meralgia paresthetica, the elusive diagnosis: Clinical experience with 14 adult patients. Ann Surg. 2000;232:281-286. 33. Dureja GP, Gulaya V, Jayalakshmi TS, Mandal, P: Management of meralgia paresthetica: A multimodality regimen. Anesth Analg. 1995;80:1060-1061. 34. Nouraei SA, Anand B, Spink G, O’Neill KS. A novel approach to the diagnosis and management of meralgia paresthetica. Neurosurgery. 2007;60:696-700. 35. Seror P. Lateral femoral cutaneous nerve conduction vs. somatosensory evoked potentials for electrodiagnosis of meralgia paresthetica. Am J Phys Med Rehabil. 1999;78:313-316. 36. Seror P. Somatosensory evoked potentials for the electrodiagnosis of meralgia paresthetica. Muscle Nerve. 2004;29:309-312. 37. Ecker A, Woltman HW. Meralgia paresthetica: A report of one hundred and fifty cases. JAMA. 1938;110:1650-1652. 38. Haim A, Pritsch T, Ben-Galim P, Dekel S. Meralgia paresthetica: A retrospective analysis of 79 patients evaluated and treated according to a standard algorithm. Acta Orthop. 2006;77:482-486. 39. Massey EW. Sensory mononeuropathies. Semin Neurol. 1998; 18:177-183. 40. Devers A, Galer BS. Topical lidocaine patch relieves a variety of neuropathic pain conditions: An open label study. Clin J Pain. 2000;16:205-208. 41. Macnichol MF, Thompson WJ. Idiopathic meralgia paresthetica. Clin Orthop Relat Res. 1990;254:270-274. 42. Nahabedian MY, Dellon AL. Meralgia paresthetica: Etiology, diagnosis and outcome of surgical decompression. Ann Plast Surg. 1995;35:590-594. 43. Edelson R, Stevens P. Meralgia paresthetica in children. J Bone Joint Surg Am. 1994;76:993-999. 44. Siu TL, Chandran KN. Neurolysis for meralgia paresthetica: An operative series of 45 cases. Surg Neurol. 2005;63:19-23. 45. van Eerten PV, Polder TW, Broere CA. Operative treatment of meralgia paresthetica: Transection versus neurolysis. Neurosugrgery. 1995;37:63-65. 46. Ivins GK. Meralgia paresthetica, the elusive diagnosis. Clinical experience with 14 adult patients. Ann Surg. 2000;232:281-286. 47. Kempe LG. Surgery of peripheral nerves: Operative exposure of the lateral femoral cutaneous nerve. In: Kempe LG. Operative Neurosurgery:Posterior Fossa, Spinal Cord, and Peripheral Nerve Disease. Berlin: Springer-Verlag; 1970, pp 208–210. 48. Aldrich EF, van den Heever CM. Suprainguinal ligament approach for surgical treatment of meralgia paresthetica: Technical note. J Neurosurg. 1989;70:492-494. 49. Patel NJ, Flashburg MH, Paskin S, Grossman R. A regional anesthetic technique compared to general anesthesia for outpatient knee arthroscopy. Anesth Analg. 1986;65:185-187.

Lower Extremity: Lateral Femoral Cutaneous Nerve Block  279 50. Reyford H, Krivosic-Horber R, Adnet P, et al. Lateral cutaneous nerve of the thigh block—155 cases. Reg Anesth. 1992;17:S47. 51. Wardrop PJ, Nishikawa H. Lateral cutaneous nerve of the thigh blockade as primary anesthesia for harvesting skin grafts. Br J Plast Surg. 1995;48:597-600. 52. Bridenbaugh PO. The lower extremity: Somatic blockade in clinical anesthesia and management of pain. Philadelphia: JB Lippincott; 1988, pp 429-431. 53. Shannon J, Lang SA, Yip RW, Gerard M. Lateral femoral cutaneous nerve block revisited: A nerve stimulator technique. Reg Anesth. 1995;20:100-104. 54. Soeding PE, Sha S, Royse CE, et al. A randomized trial of ultrasoundguided brachial plexus anesthesia in upper limb surgery. Anesth Intensive Care. 2005;33:719-725.

55. Willschke H, Marhofer P, Bösenberg A, et al. Ultrasonography for ilioinguinal/iliohypogastric nerve blocks in children. Br J Anaesth. 2005;95:226-230. 56. Tumber PS, Bhatia A, Chan VW. Ultrasound-guided lateral femoral cutaneous nerve block for meralgia paresthetica. Anesth Analg. 2008;106:1021-1022. 57. Hurdle MF, Weingarten TN, Crisostomo RA, et al. Ultrasound-guided blockade of the lateral femoral cutaneous nerve: Technical description and review of 10 cases. Arch Phys Med Rehabil. 2007;88:1362-1364. 58. Ng I, Vaghadia H, Choi PT, Helmy N. Ultrasound imaging accurately identifies the lateral femoral cutaneous nerve. Anesth Analg. 2008;107:1070-1074.

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29

Genitofemoral Neural ­Blockade Daniel E. Halpert, DO, and Alvin K. Antony, MD, FABPMR

Ilioinguinal, iliohypogastric, and genitofemoral nerves are collectively known as “border” nerves because these nerves supply the skin between the abdomen and the thigh. Because of the course of these nerves, they are at risk to injury from the lower abdominal incision (appendectomy, inguinal herniorrhaphy) or trocar insertion performed in laparoscopic surgery. Patients with neuropathic pain following injury to the nerve may present with groin pain that may extend to the scrotum or testicle in men, labia in women, and the medial aspect of the thigh. A thorough understanding of these ­“border” nerves is essential to diagnosis and treatment of neuropathic pain states related to the nerves.

Clinically Relevant Anatomy The genitofemoral nerve stems from the lumbar plexus. The lumbar plexus is formed by the ventral rami of L1 through the greater portion of L4. The ventral ramus of L1, which is frequently joined by a branch of T12, bifurcates into upper and lower portions (Fig. 29-1). The upper part divides into the iliohypogastric and ilioinguinal nerves as the lower part unites with a branch of the L2 ramus to form the genitofemoral nerve. Although much variation exists,1 the genitofemoral nerve often penetrates the psoas major muscle to then divide into a genital and femoral branch. The genital branch, or external spermatic branch, is in part responsible for the cremasteric reflex by supplying the cremaster muscle. This genital branch traverses the internal inguinal ring to descend adjacent to the spermatic cord to supply the skin of the scrotum in males. In females, it accompanies the round ligament of the uterus2 to ultimately innervate the mons pubis and labia majora. Descending on the external iliac artery and passing deep to the inguinal ligament, the femoral branch (or external lumboinguinal branch) enters the femoral sheath where it travels until it pierces the anterior layer, as well as, the fascia lata as it exits to supply skin sensation.2 Here the femoral branch supplies the skin with sensation at the anterior aspect of the femoral triangle, which is bordered by the inguinal ligament and the adductor longus and sartorius muscles. All three of the “border” nerves (the iliohypogastric, the ilioinguinal, and the genitofemoral nerves) can cross-communicate to some extent. The exact origin, course, and distribution of each individual nerve are difficult to distinguish because communication between branches exists and a high degree of variability is present.1 This cross-communication phenomena should be noted, especially if difficulty achieving successful neural blockade is experienced.

Etiology and Pathogenesis Genitofemoral neuralgia was first described in 1942.3 Injury to the genitofemoral nerve is almost always secondary to direct trauma. Direct trauma is almost always the result of surgery. Complications following inguinal herniorrhaphy4-11 and laparoscopic varicocelectomy12-16 are cited relatively frequently and can stem from inflammation, neuroma formation, deafferentation, or entrapment.4 Entrapment neuropathy can occur from impingement from staples or tacks which are used to affix the prosthetic mesh,17,18 the mesh itself, direct injury, or myofascial scarring.19 Additionally, it is not uncommon for genitofemoral neuralgia to be induced during performance of a lumbar sympathetic block.20-23 Lumbar sympathetic blocks, which are traditionally performed by injecting a needle from a posterior position toward the anterolateral aspect of the vertebral body, may allow for the injected solution to leak back along the needle shaft and spread toward the genitofemoral nerve,20 acting as a noxious irritant on the nerve. Other factors, such as an abscess or mass dwelling within or near the psoas major muscle,19 complications secondary to appendectomy,9 inguinal lymph node dissection, orchiectomy, total abdominal hysterectomy, abdominoplasty, iliac crest bone graft, femoral catheter placement,8 cesarean section,24 thermal damage following radiofrequency ablation of renal cell carcinoma,25 direct injury from an inguinal herniated mass26,27 and complications from leprosy28 have also been noted. Genitofemoral neuropathy will typically present as a neuropathic type groin pain following the distribution of the genitofemoral nerve. Pain may extend from the femoral triangle at the medial thigh to the scrotum in males or the mons pubis and labia majora in females. Although controversy exists as to which descriptors indicate a neuropathic type pain, adjectives such as “hot, burning, sensitive, and tingling” are frequently used.29

Indications Groin pain in a genitofemoral neuroanatomic distribution with neuropathic pain features is the main indication for this block. A  recent history of lower abdominal or groin trauma or surgery, especially inguinal herniorrhaphy, appendectomy, laparoscopic varicocelectomy, or cesarean section should be noted. Blocks may be used following these surgeries to augment pharmacologic pain control or during an inguinal herniorrhaphy as a local anesthetic. 281

282  Peripheral Nerve Blocks Contribution from T12 L1 Iliohypogastric

Genitofemoral nerve

Inguinal ligament

Ilioinguinal

L2

Genitofemoral

L3 Lateral femoral cutaneous L4

Femoral branch of genitofemoral nerve Genital branch of genitofemoral nerve

Psoas Pubic tubercle

Iliacus Accessory obturator Femoral nerve

L5

Figure 29-2  Genitofemoral nerve block. (From Waldman SD: Atlas of Interventional Pain Management, 2nd ed. Philadelphia, Elsevier,1998, p 305.)

Obturator

Figure 29-1  Lumbosacral anatomy of the genitofemoral nerve. (Image courtesy of Dr. Alvin K. Antony.)

Genitofemoral nerve infiltration used concomitantly with femoral nerve blocks in outpatients undergoing long saphenous vein stripping have been shown to result in a significantly faster recovery time, fewer complications, superior pain control, and better patient satisfaction when compared to spinal anesthesia.30 Diagnostically, blocks can be used to help achieve a more accurate utilization of further invasive interventions. Following failure of conservative measures of groin pain, a patient’s response to a peripheral neural blockade can be evaluated and, if temporary success is found, neurolysis,31 cryoneurolysis,32 or neurectomy33-35 may be indicated. As noted earlier, it is important to maintain an understanding of the ambiguous, overlapping distribution of the iliohypogastric, ilioinguinal, and genitofemoral nerves in the groin region and a neural blockade may need to be applied to each nerve to achieve successful pain control. Moreover, an MRI, CT, and EMG can aid in determining whether involvement of a lumbar radiculopathy, abscess, or malignancy exists.

Technique Multiple techniques exist to access the branches of the genitofemoral nerve. Traditionally, the patient is placed supine and major anatomic landmarks including the anterior superior iliac spine, pubic tubercle, inguinal ligament, inguinal or femoral crease, and femoral artery are identified by palpation. If pain is experienced from nerve traction, a pillow may be placed underneath the patient’s knees to

induce hip flexion and alleviate the tension placed at the anterior aspect of the groin. The genital branch is blocked by locating a point immediately lateral to the pubic tubercle and inferior to the inguinal ligament (Fig. 29-2). Following sterilization of the skin in this area, a 1.5- to 2-inch needle containing 5 to 10 mL of 1% preservative-free lidocaine is injected through the skin and subcutaneous area subsequent to aspiration.19,30,36 If an inflammatory component is noted, 40 to 80 mg of methylprednisolone or triamcinolone can be added to augment the anesthetic solution.36 A trans-psoas technique, in which the patient lies prone and a 5- to 6-inch 21- to 22-gauge needle is introduced paravertebrally, approximately 5 cm from midline at the level of the L3-L4 interspace, is also used. The needle is then advanced toward the transverse process of either L3 or L4 and the depth of the transverse process is noted. The needle is withdrawn and marked at twice the depth of the transverse process. It is then reinserted to pass perpendicularly between the transverse processes and through the quadratus lumborum where loss of resistance will identify the first psoas muscle compartment. The needle continues to be further advanced until a second loss of resistance is noted, indicating the space located anteriorly to the psoas major muscle. Here, 2 to 3 mL of local anesthetic is deposited.19,37 An alternative technique for blocking the genital branch under high-frequency ultrasound guidance has been suggested as being superior when compared to the traditional blind method. As explained by Peng38: “The orientation of the (linear) probe is perpendicular to the inguinal ligament. The final position of the probe is about 1 fingerbreadth lateral to the pubic tubercle. However, inexperienced practitioners may have difficulty visualizing the spermatic cord, which is oval or circular in shape with 1 or 2 arteries within it (the testicular artery and the artery to vas deferens). The vas deferens is often seen as a thick tubular structure within the spermatic cord. It is suggested to start scanning with the probe in the internal inguinal ring,

Genitofemoral Neural Blockade  283

at which the femoral artery can be visualized in the longitudinal scan (along the length of the femoral artery). By moving the probe in the cephalad direction, the artery is seen as diving deep toward the inguinal ligament. At this point, an oval or circular structure can easily be seen superficial to the femoral artery. The probe is then moved slightly in the medial direction away from the femoral artery. An out-of-plane technique is also used with the needle approaching the skin from the lateral aspect of the probe.” When correctly positioned, 5 mL of local anesthetic deposited inside and 5 mL deposited outside the spermatic cord should then take place. This external deposit is to ensure access because anatomic anomalies of the genital branch location are often encountered.38 The femoral branch can be blocked by implementing a fanlike infiltration into the subcutaneous tissue of 10 to 15 mL of local anesthetic in the medial, caudad, and cephalad direction at the lateral border of the femoral artery at the inguinal crease.19

Contraindications Contraindications to injection therapy can be broadly divided into absolute and relative contraindications. As with any form of injection therapy, allergy to the local anesthetic is an absolute contraindication for its use. Furthermore, cellulitis over the area to be injected is reason to postpone a nerve block. Other absolute infectious contraindications include any localized or systemic infection or sepsis. Relative contraindications include immunosuppressed states due to medications (chemotherapeutics, immunomodulating medications, or systemic steroids) or disease (AIDS, leukemia). Diabetes, because of its association with poor wound healing, risk of infection as well as potential for steroid-induced hyperglycemia is reason for caution. The use of anticoagulation therapy has been cautioned widely when performing nerve blocks, and the American Society for Regional Anesthesia (ASRA) has published guidelines. As with all interventions, a patient’s unwillingness to provide informed consent is an absolute contraindication to the procedure.

Complications Common complications of a genitofemoral neuroblockade are localized pain at the injection site, ecchymosis, and hematoma formation. As expected, the latter two are more probable if anticoagulation is being used simultaneously. Direct pressure should be applied over the injection site to help prevent this occurrence. Infection anywhere along the injection site may occur and careful consideration should be applied when preparing the skin for sterilization prior to injection. When needle insertion occurs, depth of advancement should be meticulously monitored because penetration of the peritoneal cavity with a subsequent bowel perforation can induce bacterial contamination with a resultant peritonitis and fistula formation. For obvious reasons, care should be taken to avoid piercing the femoral artery, testicular artery, and vas deferens.

Treatment Options Other treatments to help manage pain induced by genitofemoral neuropathy are mentioned in the literature. Gabapentin, a calcium channel alpha2-delta ligand, may play a beneficial role39 and is indicated for first-line treatment in neuropathic pain management.40

A peripheral nerve stimulator, which requires placement directly on the nerve, has been shown to be effective in the treatment of genitofemoral neuralgia secondary to hernioplasty.41 Additional options that have been shown to be effective are neurolysis,31 cryoanalgesia (the application of cold to nerve tissues for the purpose of disrupting nerve structures but maintaining the myelin sheath and endoneurium intact),32 and neurectomy.11,33,34

Conclusion Genitofemoral nerve blocks provide valuable diagnostic and therapeutic information about patients suffering with neuropathic pain in the border territory between the abdomen and pelvis and the groin area. Because of anatomic variations, techniques that rely on surface anatomy may be prone to greater failure than techniques that use ultrasonography. Ultrasonography allows visualization of the nerves or the structures important to the identification of the nerves and provides the opportunity for selective real-time injections. REFERENCES   1. Rab M, Ebmer J, Dellon AL. Anatomic variability of the ilioinguinal and genitofemoral nerve: Implications for the treatment of groin pain. Plast Reconstr Surg. 2001;108(6):1618-1623.   2. Gray H, Lewis WH. Anatomy of the Human Body. 20th ed. Philadelphia: Lea & Febiger; 1918.   3. Magee RK. Genitofemoral causalgia: A new syndrome. Can Med Assoc J. 1942;46:326-329.   4. Rho RH, Lamer TJ, Fulmer JT. Treatment of genitofemoral neuralgia after laparoscopic inguinal herniorrhaphy with fluoroscopically guided tack injection. Pain Med. 2001;2(3):230-233.   5. Aroori S, Spence RA. Chronic pain after hernia surgery—an informed consent issue. Ulster Med J. 2007;76(3):136-140.   6. Starling JR, Harms BA, Schroeder ME, Eichman PL. Diagnosis and treatment of genitofemoral and ilioinguinal entrapment neuralgia. Surgery. 1987;102(4):581-586.   7. Aasvang E, Kehlet H. Surgical management of chronic pain after inguinal hernia repair. Br J Surg. 2005;92(7):795-801.   8. Nahabedian MY, Dellon AL. Outcome of the operative management of nerve injuries in the ilioinguinal region. J Am Coll Surg. 1997;184(3):265-268.   9. Lyon EK. Genitofemoral causalgia. Can Med Assoc J. 1945;53:213-216. 10. Tetik C, Arregui ME, Dulucq JL, et al. Complications and recurrences associated with laparoscopic repair of groin hernias. A multi-­institutional retrospective analysis. Surg Endosc. 1994;8(11): 1316-1322. 11. Harms BA, DeHaas Jr DR, Starling JR. Diagnosis and management of genitofemoral neuralgia. Arch Surg. 1984;119(3):339-341. 12. Chrouser K, Vandersteen D, Crocker J, Reinberg Y. Nerve injury after laparoscopic varicocelectomy. J Urol. 2004;172(2):691-693. 13. Jarow JP, Assimos DG, Pittaway DE. Effectiveness of laparoscopic varicocelectomy. Urology. 1993;42(5):544-547. 14. Muensterer OJ. Genitofemoral nerve injury after laparoscopic varicocelectomy in adolescents. J Urol. 2008;180(5):2155-2157. 15. Poulsen EU, Willumsen H, Colstrup H, Jensen KM. Varicocele of the testis. A comparison between laparoscopic and conventional surgery. Ugeskr Laeger. 1994;156(39):5683-5685. 16. Podkamenev VV, Stalmakhovich VN, Urkov PS, et al. Laparoscopic surgery for pediatric varicoceles: Randomized controlled trial. J Pediatr Surg. 2002;37(5):727-729. 17. Seid AS, Amos E. Entrapment neuropathy in laparoscopic herniorrhaphy. Surg Endosc. 1994;8(9):1050-1053. 18. Rosenberger RJ, Loeweneck H, Meyer G. The cutaneous nerves encountered during laparoscopic repair of inguinal hernia: New anatomical findings for the surgeon. Surg Endosc. 2000;14(8):731-735.

29

284  Peripheral Nerve Blocks 19. Vloka JD, Hadzic A. Obturator and Genitofemoral Nerve Blocks. Tech Reg Anesth Pain Manag. 1999;3(1):28-32. 20. Datta S, Pai U. Paradiscal extraforaminal technique for lumbar sympathetic block: Report of a proposed new technique utilizing a cadaver study. Pain Physician. 2004;7(1):53-57. 21. Sayson SC, Ramamurthy S, Hoffman J. Incidence of genitofemoral nerve block during lumbar sympathetic block: Comparison of two lumbar injection sites. Reg Anesth. 1997;22(6):569-574. 22. Dirim A, Kumsar S. Iatrogenic ureteral injury due to lumbar sympathetic block. Scand J Urol Nephrol. 2008;4:395-396. 23. Kim WO, Yoon KB, Kil HK, Yoon DM. Chemical lumbar sympathetic block in the treatment of plantar hyperhidrosis: A study of 69 patients. Dermatol Surg. 2008;34(10):1340-1345. 24. Ducic I, Moxley M, Al-Attar A. Algorithm for treatment of postoperative incisional groin pain after cesarean delivery or hysterectomy. Obstet Gynecol. 2006;108(1):27-31. 25. Boss A, Clasen S, Kuczyk M, et al. Thermal damage of the genitofemoral nerve due to radiofrequency ablation of renal cell carcinoma: A potentially avoidable complication. AJR Am J Roentgenol. 2005;185(6):1627-1631. 26. Bademkiran F, Tataroglu C, Ozdedeli K, et al. Electrophysiological evaluation of the genitofemoral nerve in patients with inguinal hernia. Muscle Nerve. 2005;32(5):600-604. 27. Soyer T, Tosun A, Aydin G, et al. Evaluation of genitofemoral nerve motor conduction in inguinoscrotal pathologies. J Pediatr Surg. 2008;43(8):1540-1542. 28. Agrawal SK, Singal A, Pandhi D, Oberoi S. Involvement of genitofemoral nerve with genital lesions in lepromatous leprosy. Indian J Lepr. 2004;76(1):71-77. 29. Jensen MP. Review of measures of neuropathic pain. Curr Pain Headache Rep. 2006;10(3):159-166. 30. Vloka JD, Hadzic A, Mulcare R, et al. Femoral and genitofemoral nerve blocks versus spinal anesthesia for outpatients undergoing long saphenous vein stripping surgery. Anesth Analg. 1997;84(4):749-752.

31. Weksler N, Klein M, Gurevitch B, et al. Phenol neurolysis for severe chronic nonmalignant pain: Is the old also obsolete? Pain Med. 2007;8(4):332-337. 32. Trescot AM. Cryoanalgesia in interventional pain management. Pain Physician. 2003;6(3):345-360. 33. Murovic JA, Kim DH, Tiel RL, Kline DG. Surgical management of 10 genitofemoral neuralgias at the Louisiana State University Health Sciences Center. Neurosurgery. 2005;56(2):298-303. 34. Krahenbuhl L, Striffeler H, Baer HU, Buchler MW. Retroperitoneal endoscopic neurectomy for nerve entrapment after hernia repair. Br J Surg. 1997;84(2):216-219. 35. Kennedy EM, Harms BA, Starling JR. Absence of maladaptive neuronal plasticity after genitofemoral-ilioinguinal neurectomy. Surgery. 1994;116(4):665-670. 36. Waldman SD. Atlas of Interventional Pain Management. 2nd ed. Philadelphia: Elsevier; 1998, p 302. 37. Hartrick CT. Genitofemoral nerve block: A transpsoas technique. Reg Anesth. 1994;19(6):432-433. 38. Peng PW, Tumber PS. Ultrasound-guided interventional procedures for patients with chronic pelvic pain—a description of techniques and review of literature. Pain Physician. 2008;11(2):215-224. 39. Benito-Leon J, Picardo A, Garrido A, Cuberes R. Gabapentin therapy for genitofemoral and ilioinguinal neuralgia. J Neurol. 2001;248(10):907-908. 40. Dworkin RH, O’Connor AB, Backonja M, et al. Pharmacologic management of neuropathic pain: Evidence-based recommendations. Pain. 2007;132(3):237-251. 41. Walter J, Reichart R, Vonderlind C, Kuhn SA, Kalff R. Neuralgia of the genitofemoral nerve after hernioplasty: Therapy by peripheral nerve stimulation. Chirurg. 2009;80(8):741-744.

Ilioinguinal and Iliohypogastric Neural Blockade

30

SriKrishna Chandran, MD, and Alvin K. Antony, MD, FABPMR

Ilioinguinal, iliohypogastric, and genitofemoral nerves are collectively known as “border nerves” because these nerves supply the skin between the abdomen and the thigh. Because of the course of these nerves, they are at risk to injury from the lower abdominal incision (appendectomy, inguinal herniorrhaphy) or trocar insertion performed in laparoscopic surgery. Patients with neuropathic pain following injury to the nerve may present with groin pain that may extend to the scrotum or testicle in men, labia in women, and the medial aspect of the thigh. A thorough understanding of these “border” nerves is essential to diagnosis and treatment of neuropathic pain states related to the nerves.

Clinically Relevant Anatomy The ilioinguinal and iliohypogastric nerves are branches of the lumbar plexus originating from the ventral ramus of L1 with occasional contributing fibers from T12 (Fig. 30-1). They emerge from the superolateral border of the psoas major muscle, course posterior to the medial arcuate ligaments, and anterolateral to the quadratus lumborum. Above the anterior superior iliac spine (ASIS), they pierce the transverse abdominal muscle or transversus abdominus.1,2 The iliohypogastric nerve continues between the transversus abdominis and internal oblique, dividing into lateral and anterior cutaneous branches. The lateral cutaneous branch perforates the internal and external oblique muscle above the iliac crest and innervates the posterolateral gluteal skin. The anterior cutaneous branch runs medial to the anterior superior iliac spine, perforating the external oblique aponeurosis above the superficial inguinal ring and innervating the suprapubic skin.1,2 The ilioinguinal nerve travels through the internal oblique muscle, traversing the inguinal canal below the spermatic cord. It exits through the superficial inguinal ring to innervate the proximal medial skin of the thigh. In males, it innervates the skin over the penile root and the upper scrotum. In females, it innervates the skin covering the mons pubis and the adjoining labia majora.1,2 The iliohypogastric and ilioinguinal nerves occasionally interconnect along their courses, resulting in variations in the dermatomal distribution.3

Etiology and Pathogenesis The vast majority of ilioinguinal and iliohypogastric neuralgias are iatrogenic. In 1942, Magee first described ilioinguinal and iliohypogastric neuralgias in scientific literature.4 Since then, a variety of

etiologies have been detailed. Ilioinguinal and iliohypogastric neuropathies have been associated with a variety of lower abdominal surgeries.5 They may be the result of entrapment from sutures or staples, or result from adhesions, scarring, or inflammation. Neuroma formation, resulting from electrocauterization or laceration during open/laparoscopic procedures, may also contribute to this process. Ilioinguinal and iliohypogastric neuralgias have been reported after various surgical procedures such as inguinal herniorrhaphy, appendectomy, abdominoplasty, needle bladder suspension, and iliac crest bone harvesting.6-9 A variety of obstetric surgical interventions such as total abdominal hysterectomy, pelvic lymphadenectomy, bilateral salpingo-oophorectomy, and other procedures involving Pfannenstiel incisions have also been associated with ilioinguinal and iliohypogastric neuralgias.10-13 The pathogenesis of these neuralgias depends on the etiology. In the case of entrapment, chronic compression may result in demyelination and axonal damage. A build-up of connective tissue in the endoneurium and perineurium may cause nerve thickening distal to the site of entrapment. In turn, this may affect the vascular supply through the vasa nervorum as well as axonal transport; ultimately disrupting neural function. Impulse generation and conduction may be affected causing symptoms.14 Neuroma formation may result from a transection of the nerve. When this occurs, the resulting axonal ends may continue to grow in a disorganized fashion. This, in turn, may result in a bulbous collection of unmyelinated fibers. These neuromas are far more mechanosensitive and thermosensitive than normal nerve endings and may produce spontaneous discharges resulting in neuropathy.15 A diagnostic triad for ilioinguinal and iliohypogastric neuralgias include neuropathic pain classically described as a burning, sharp, or lancinating sensation along the distribution of the affected nerve, hyperesthesia or hypoesthesia to the area supplied by the nerve, and pain relief by infiltration with anesthetic at the site where maximum pain occurs.

Indications Ilioinguinal and iliohypogastric nerve blocks are used as a diagnostic and therapeutic tool in the management of ilioinguinal and iliohypogastric neuropathies. They are used to determine true neuropathy, discriminate peripheral nerve pathology from radiculopathy, as well as to treat both chronic and acute groin pain. In addition, they may help to predict the outcome of permanent corrections such as neurectomy and neurolysis. 285

286  Peripheral Nerve Blocks Contribution from T12 L1 Iliohypogastric Ilioinguinal

L2

Genitofemoral

X a L3

Lateral femoral cutaneous L4 Psoas Iliacus Accessory obturator Femoral nerve

L5

Obturator

Figure 30-1  Lumbosacral anatomy. (Image courtesy of Dr. Alvin K. Antony.)

In combination with pharmacologic management, ilioinguinal and iliohypogastric blocks have been used to provide analgesia following surgeries such as inguinal herniorrhaphies, cesarean sections, orchiopexy, and total abdominal hysterectomies.16-19 In patients with chronic groin pain resulting from neuralgia, ilioinguinal and iliohypogastric nerve blocks have provided analgesia following failure of more conservative therapies.20

Technique The standard technique for performing ilioinguinal and iliohypogastric nerve blocks places the patient in the supine position. The patient is exposed from the umbilicus to the upper thigh. A  pillow may be placed under the patient’s knees to prevent complete hip extension, exacerbating the pain in some instances. Surface anatomic landmarks include the anterior superior iliac spine and pubic tubercle which are identified by palpation. The skin is then sterilized. A 25-gauge to 27-gauge needle, which is 2.5 cm to 7.5 cm in length, may be used—depending on the size of the patient. The first technique described relies on anatomic landmarks; the nerves are typically blocked 2 cm medial and superior to the anterior superior iliac spine (Fig. 30-2) along a line connecting the ASIS and the umbilicus. Here, the needle is inserted perpendicularly to the skin, noting penetration of each muscle fascial layer. Local anesthetic (10 mL with corticosteroid agent—typically methylprednisolone or triamcinolone 40 to 80 mg) is applied.

Figure 30-2  Surface anatomy image demonstrating the anterior ­superior iliac spine (ASIS); proper needle insertion point for an ilioinguinal/­ iliohypogastric block (X) 2 cm superior and medial to the ASIS.

Recently, ultrasonography has been used to better visualize the ilioinguinal and iliohypogastric nerves in the performance of these blocks. Although the literature on the efficacy and utility of this technique is growing, it remains an area of study. In the second technique, a linear probe of high frequency may be used because it provides good visualization of fascial and superficial structures.22 The probe is typically oriented obliquely, perpendicular to the inguinal ligament and to the anatomic course of both nerves. In this position, the probe is oriented roughly parallel to the abdominal muscle fibers, thereby improving image quality.22,23 The inferolateral part of the transducer may be placed slightly above the anterior superior iliac spine. Key structures to visualize include the anterior superior iliac spine, the peritoneum, the transversus abdominis, the internal oblique, and the external oblique.22-25 After identification of the ilioinguinal and iliohypogastric nerves, the block is performed using the out-of-plane (OOP) technique. With this technique, the needle is inserted perpendicular to the face of the transducer. With proper technique, it is possible to place the tip of the needle between the ilioinguinal and iliohypogastric nerves and inject about 10 mL of local anesthetic to achieve an adequate distribution. In chronic pain patients, it is possible to distinguish whether a pain syndrome is caused by either the ilioinguinal or iliohypogastric nerves by blocking each nerve with 1 mL of local anesthetic. For this purpose, diffusion of local anesthetic along a fascial plane should be avoided. Figure 30-3 demonstrates an ultrasound probe just above the ASIS with the needle inserted medial to the ASIS. Figure 30-4 demonstrates an ultrasound image of the anatomic structures at the level of the ASIS. On visualization of the key anatomic landmarks, the agent is injected between the internal oblique abdominal muscle and transverse abdominal muscle layers.22 It is worth noting that a branch of the deep circumflex artery lies between the internal oblique abdominal muscle and the transverse abdominal muscle, in the same plane as the ilioinguinal and iliohypogastric nerves.25 This has been suggested as a landmark in performing ultrasound-guided ilioinguinal and iliohypogastric nerve blocks. Injection of agent adjacent to this artery may result in anesthesia of both nerves.25 Use of power Doppler while using ultrasound will help localize this vascular structure. Avoid intra-arterial injection by aspiration prior to the injection of ­anesthetic/steroid agent.

Ilioinguinal and Iliohypogastric Neural Blockade  287

30 EOAM IOAM

IIN

TAM IHN

Figure 30-3  Image depicts needle position relative to the ultrasound probe for the ilioinguinal/iliohypogastric nerve block. (From Willschke H, Marhofer P, Bosenberg A, et al: Ultrasonographic-guided ilioinguinal/iliohypogastric nerve block in pediatric anesthesia: what is the optimal volume? Anesth Analg. 2006;102:1680-1684.)

Figure 30-4  Ultrasound illustration of the lateral abdominal wall at the level of the anterior superior iliac spine (left). EOAM, external oblique abdominal muscle; IOAM, internal oblique abdominal muscle; IHN, iliohypogastric nerve; IIN, ilioinguinal nerve; TAM, transverse abdominal muscle. (Image courtesy of Dr. Alvin K. Antony.)

It should be noted that in some individuals a genitofemoral nerve block may further alleviate pain. In the event that this too fails to improve symptoms, studies including electrodiagnostic studies and magnetic resonance imaging may be warranted to evaluate for radiculopathy, malignancy, or abscess formation.27

insertion can minimize this risk. The peritoneum lies just below the fascia and is therefore at risk for penetration. This may subsequently result in peritonitis, bowel perforation, or fistula formation. Other complications include paresthesias of the lower limb, intravascular injection, or inadvertent femoral nerve block.

Contraindications Contraindications to injection therapy can be broadly divided into absolute and relative contraindications. As with any form of injection therapy, allergy to the local anesthetic is an absolute contraindication to its use. Furthermore, cellulitis over the area to be injected is reason to postpone a nerve block. Other absolute infectious contraindications include any localized or systemic infection or sepsis. Relative contraindications include immunosuppressed states either due to medications (chemotherapeutics, immunomodulating medications, or systemic steroids) or disease (AIDS, leukemia). Diabetes, due to its association with poor wound healing, risk of infection as well as potential for steroid-induced hyperglycemia is reason for caution. The use of anticoagulation therapy has widely been cautioned when performing nerve blocks, and the American Society for Regional Anesthesia (ASRA) has published guidelines. Finally, as with all interventions, a patient’s unwillingness to provide informed consent is an absolute contraindication to the procedure.

Complications While both ilioinguinal and iliohypogastric nerve blocks are safe procedures, they have been associated with some complications including bleeding with hematoma formation or ecchymosis. This may be more likely in patients with any existing blood dyscrasia or in those who are on concurrent anticoagulation. The risk of bleeding may be minimized by placing constant pressure to the area of incision following the procedure. Infection is another important risk. Maintaining sterile technique and using caution in needle

Treatment Options Ilioinguinal and iliohypogastric neuralgias may be treated using a variety of medications and techniques. Commonly used medications to treat neuropathic pain include gabapentin, pregabalin, tricyclic antidepressants, and duloxetine (Cymbalta).28-30 Gabapentin is an alpha2-delta ligand thought to act on the voltage-gated calcium channel.28,30 Pregabalin binds with high affinity to the alpha2-delta site (an auxiliary subunit of voltage-gated calcium channels) in central nervous system (CNS) tissues. Binding to the alpha2-delta subunit may be involved in pregabalin’s antinociceptive and antiseizure effects in animal models. The exact mechanism of action of pregabalin is unknown.28,30 Tricyclic antidepressants are thought to affect pain pathways through their inhibition of serotonin and norepinephrine reuptake, affinity for the histamine H1-receptor, and effects on sodium channels.28,30 Although the exact mechanisms of the antidepressant, central pain inhibitory and anxiolytic actions of duloxetine in humans are unknown, these actions are believed to be related to its potentiation of serotonergic and noradrenergic activity in the CNS.28,30 Other options for treatment of neuropathic pain include implantation of peripheral nerve stimulators, spinal cord stimulation, and surgical neurectomy.31-37 In cases of well-defined neuromas that respond to anesthetic blocks, surgical neurectomy may be the preferred first line of therapy after medications.39 Surgical treatment involves the abatement of neuroma pain by relocating the painful neuroma to areas of low mechanical stress. The implied mechanism is that mechanically tethered neuromas produce pain when subjected to mechanical stress near joints, scars, and structures with wide range of motion. Nerves may be cut back and implanted in healthy, well-vascularized muscle. The cut

288  Peripheral Nerve Blocks

ends may again sprout and a new neuroma may form. However, the chances are reduced that the nerve will be subject to tension and shearing forces which are likely to play a role in neuropathic pain generation.39

Conclusion Ilioinguinal and iliohypogastric nerve blocks provide valuable diagnostic and therapeutic information about patients suffering with neuropathic pain in the border territory between the abdomen and pelvis and the groin area. Because of anatomic variations, techniques that rely on surface anatomy may be prone to greater failure than techniques that use ultrasonography. Ultrasonography allows visualization of the nerves or the structures important to the identification of the nerves and provides the opportunity for selective injection and real-time injections. REFERENCES   1. Standring S. Posterior abdominal wall and retroperitoneum. In: Gray H, Standring S, Ellis H, Berkovitz BKB, eds. Gray’s Anatomy: The Anatomical Basis of Clinical Practice. London: Elsevier Churchill Livingstone; 2005:1113.   2. Moore KL, Dalley AF. Abdomen. In: Kelly PJ, ed. Clinically Oriented Anatomy. 5th ed. Baltimore: Lippincott Williams & Wilkins; 2006:207.   3. al-dabbagh AK. Anatomical variations of the inguinal nerves and risks of injury in 110 hernia repairs. Surg Radiol Anat. 2002;24(2):102-107.   4. Magee RK. Genitofemoral causalgia: A new syndrome. Can Med Assoc J. 1942(46):326-329.   5. Waldman SD. Ilioinguinal-iliohypogastric and genitofemoral nerve blocks. In: Lampert R, ed. Interventional Pain Management. 2nd ed. Philadelphia: WB Saunders; 2001:508.   6. Liszka TG, Dellon AL, Manson PN. Iliohypogastric nerve entrapment following abdominoplasty. Plast Reconstr Surg. 1994;93(1):181-184.   7. Melville K, Schultz EA, Dougherty JM. Ilionguinal-iliohypogastric nerve entrapment. Ann Emerg Med. 1990;19(8):925-929.   8. Monga M, Ghoniem GM. Ilioinguinal nerve entrapment following needle bladder suspension procedures. Urology. 1994;44(3):447-450.   9. Bents RT. Ilioinguinal neuralgia following anterior iliac crest bone harvesting. Orthopedics. 2002;25(12):1389-1390. 10. Cardosi RJ, Cox CS, Hoffman MS. Postoperative neuropathies after major pelvic surgery. Obstet Gynecol. 2002;100(2):240-244. 11. El-Minawi AM, Howard FM. Iliohypogastric nerve entrapment following gynecologic operative laparoscopy. Obstet Gynecol. 1998;91:871. 12. Sippo WC, Burghardt A, Gomez AC. Nerve entrapment after Pfannenstiel incision. Am J Obstet Gynecol. 1987;157(2):420-421. 13. Tosun K, Schafer G, Leonhartsberger N, et al. Treatment of severe bilateral nerve pain after Pfannenstiel incision. Urology. 2006;67(3):623:e5,623.e6. 14. Seid AS, Amos E. Entrapment neuropathy in laparoscopic herniorrhaphy. Surg Endosc. 1994;8(9):1050-1053. 15. Benzon HT, Raja SN, Molloy RE, et al. Truncal blocks. In: Andjelkovic N, ed. Essentials of Pain Medicine and Regional Anesthesia. Philadelphia: Elsevier, Churchill Livingstone; 2005:636. 16. Abad-Torrent A, Calabuig R, Sueiras A, et al. Efficacy of the ilioinguinal and iliohypogastric block in the treatment of the postoperative pain of inguinal herniorrhaphy. Rev Esp Anestesiol Reanim. 1996;43(9):318-320. 17. Oriola F, Toque Y, Mary A, et al. Bilateral ilioinguinal nerve block decreases morphine consumption in female patients undergoing

nonlaparoscopic gynecologic surgery. Anesth Analg. 2007;104(3): 731-734. 18. Lipp A. Ilioinguinal nerve block for orchidopexy. Anaesthesia. 1998;53(5):515-516. 19. Gucev G, Yasui GM, Chang TY, Lee J. Bilateral ultrasound-guided continuous ilioinguinal-iliohypogastric block for pain relief after cesarean delivery. Anesth Analg. 2008;106(4):1220. 20. Miyazaki F, Shook G. Ilioinguinal nerve entrapment during needle suspension for stress incontinence. Obstet Gynecol. 1992;80(2):246-248. 21. Choi PD, Nath R, Mackinnon SE. Iatrogenic injury to the ilioinguinal and iliohypogastric nerves in the groin: A case report, diagnosis, and management. Ann Plast Surg. 1996;37(1):60-65. 22. Hu P, Harmon D, Frizelle H. Ultrasound guidance for ilioinguinal/­ iliohypogastric nerve block: A pilot study. Ir J Med Sci. 2007;176(2): 111-115. 23. Eichenberger U, Greher M, Kirchmair L, et al. Ultrasound-guided blocks of the ilioinguinal and iliohypogastric nerve: Accuracy of a selective new technique confirmed by anatomical dissection. Br J Anaesth. 2006;97(2):238-243. 24. Peng PW, Tumber PS. Ultrasound-guided interventional procedures for patients with chronic pelvic pain—a description of techniques and review of literature. Pain Physician. 2008;11(2):215-224. 25. Gofeld M, Christakis M. Sonographically-guided ilioinguinal nerve block. J Ultrasound Med. 2006;25(12):1571-1575. 26. Waldman SD. Atlas of Interventional Pain Management. 2nd ed. Philadelphia: WB Saunders; 2004, 294–300. 27. Gallagher RM. Management of neuropathic pain: Translating mechanistic advances and evidence-based research into clinical practice. Clin J Pain. 2006;(Suppl 1):S2-8. 28. Benito-Leon J, Picardo A, Garrido A, Cuberes R. Gabapentin therapy for genitofemoral and ilioinguinal neuralgia. J Neurol. 2001;248(10):907-908. 29. Dworkin RH, O’Connor AB, Backonja M, et al. Pharmacologic management of neuropathic pain: Evidence-based recommendations. Pain. 2007;132(3):237-251. 30. Rauchwerger JJ, Giordano J, Rozen D, et al. On the therapeutic viability of peripheral nerve stimulation for ilioinguinal neuralgia: Putative mechanisms and possible utility. Pain Pract. 2008;8(2):138-143. 31. Pappalardo G, Frattaroli FM, Mongardini M, et al. Neurectomy to prevent persistent pain after inguinal herniorraphy: A prospective study using objective criteria to assess pain. World J Surg. 2007;31(5):1081-1086. 32. Tsakayannis DE, Kiriakopoulos AC, Linos DA. Elective neurectomy during open, “tension free” inguinal hernia repair. Hernia. 2004;8(1):67-69. 33. Trescot AM. Cryoanalgesia in interventional pain management. Pain Physician. 2003;6(3):345-360. 34. Rozen D, Ahn J. Pulsed radiofrequency for the treatment of ilioinguinal neuralgia after inguinal herniorrhaphy. Mt Sinai J Med. 2006;73(4):716-718. 35. Amid PK. Causes, prevention, and surgical treatment of postherniorrhaphy neuropathic inguinodynia: Triple neurectomy with proximal end implantation. Hernia. 2004;8(4):343-349. 36. Whiteside JL, Barber MD. Ilioinguinal/iliohypogastric neurectomy for management of intractable right lower quadrant pain after cesarean section: A case report. J Reprod Med. 2005;50(11):857-859. 37. Willschke H, Bosenberg A, Marhofer P. Ultrasonographic-guided ilioinguinal/iliohypogastric nerve block in pediatric anesthesia: What is optimal volume. Anesth Analg. 2006;102:1680-1684. 38. Loeser JD, Butler SH, Chapman R, Turk DC. Bonica’s Management of Pain. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001: 2013–2014.

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Intercostal Nerve Block Li Zhang, MD, PhD, and Aneesh K. Singla, MD, MPH Intercostal nerve block can be useful in the management of acute and chronic pain, thoracic radicular pain, or chest wall pain. It is performed with or without image guidance. This chapter describes the anatomy, nerve block technique, and potential complications.

Anatomy of Intercostal Nerves The twelve pairs of thoracic spinal nerves (T1-12) are divided into ventral and dorsal rami after they pass through the intervertebral foramina. The ventral rami of T1-T11 form the intercostal nerves that enter the intercostal spaces. The ventral ramus of T12 forms the subcostal nerve that is located inferior to the 12th rib. The dorsal rami of T1-T12 pass posteriorly to supply sensation to skin, muscles, and bones of the back.1 Intercostal nerves are composed of dorsal horn sensory afferent fibers, ventral horn motor efferent fibers, and postganglionic sympathetic nerves. The major branches of intercostal nerves are anterior and lateral cutaneous branches (Fig. 31-1). These branches divide and innervate the skin and intercostal muscles of an individual segment along with variable collateral innervation of the adjacent segments. Because of such collateral innervation, it is necessary to block a level above and below the desired level when an intercostal nerve block is performed. Throughout its course, each intercostal nerve is associated with an artery and a vein. The intercostal arteries are derived directly from the aorta. The intercostal veins are derived from the confluence of venules along the chest and end in the azygous and hemiazygous veins. The intercostal nerve travels inferior to the vein and artery of the same segment (Fig. 31-2).

Pathophysiology of Intercostal Neuralgia The pathogenesis of acute intercostal neuralgia involves multiple etiologies, such as skin and muscle injury, costochondral dislocation, costovertebral ligament damage, postherpetic neuralgia, postthoracotomy pain, or intercostal neuritis. The pathophysiology of acute pain involves chemosensitive ion channels in peripheral nociceptors that are activated by cytokines released from damaged tissue or inflammatory cells. Activation of these channels results in generation of action potentials that are conducted from the peripheral nociceptors in the chest area to the thoracic spinal cord via intercostal nerves. The pathophysiology of chronic intercostal neuralgia pain is complex and involves a combination of peripheral, central, and psychological mechanisms. In some patients, a structural or

inflammatory source can be identified; however, most patients encountered in clinical practice have primary pain disorders in which the etiologies are uncertain.

Indications for Intercostal Nerve Blocks An intercostal nerve block is used for therapeutic and diagnostic purposes. Intercostal nerve blocks manage acute and chronic pain in the chest area. Common indications for an intercostal nerve block are described subsequently. Chest wall surgery: An intercostal block with a single injection or an indwelling catheter offers analgesia for thoracotomy and percutaneous drainage tubes. It also helps relieve pain after upper abdominal or flank surgery. Chest wall trauma: Single injections around the appropriate intercostal nerves or continuous infusion with intercostal catheters helps to control pain resulting from fractured ribs and other chest wall trauma. Shingles or postherpetic neuralgia: An intercostal nerve block(s) is used to treat pain caused by shingles—an acute via herpes-zoster infection resulting in inflammation of the intercostal nerves and dorsal root ganglion. Chronic conditions: An intercostal nerve block is helpful in the management of pain associated with chest wall tumors, nerve entrapment syndromes, thoracic spine pain, and intercostal neuralgia. Diagnostic nerve block: An intercostal block is often performed to determine if an intercostal nerve is involved in the generation of chest wall pain. If an intercostal block via a single injection is able to provide temporary pain relief, it indicates that the intercostal nerve is likely a component of that pain pathway. Subsequently, a neurolytic block, cryoablation, radiofrequency ablation, or chemical neurolysis can be performed in the same intercostal segment to relieve pain for an extended period of time.

Technique An intercostal nerve block can be performed with the patient in a sitting, prone, or lateral decubitus position and the intended block region upward. Sedation is optional and can be achieved with a combination of a benzodiazepine, a short-acting narcotic such as fentanyl, and/or ketamine. The insertion site for an intercostal nerve block is usually just below the lower edge of the rib, slightly medial to the posterior 289

290  Peripheral Nerve Blocks Superior costotransverse ligament Lateral branch Medial branch Posterior intercostal membrane Subcostalis muscle Dorsal ramus Rami communicantes

Intercostal nerve (ventral ramus)

Sympathetic ganglion Lateral cutaneous branch Intercostalis intimus muscle Internal intercostal muscle Pleura External intercostal muscle

Anterior cutaneous branch Figure 31-1  Anatomy of an intercostal nerve. (Adapted from Ferrante FM, VadeBoncouer TR: Postoperative Pain Management. New York, Churchill Livingstone, 1993. Elsevier.) A N G L E

O F R I B

Branch 3 Dorsal rami

LATERAL

Branch 4 Lateral Branches 1, 2 Innermost cutaneous br. Gray and white intercostal m. Internal rami communicantes intercostal m. Vein Artery Nerve Intercostal m. External Internal Innermost Branch 5 Anterior cutaneous br.

Figure 31-2  Intercostal nerve block: Cross-sectional anatomy. (From Brown DL: Atlas of Regional Anesthesia, 3rd ed. Philadelphia, Saunders 2006, p 240.).

Intercostal Nerve Block  291

axillary line, and 6 to 8 cm lateral to the respective vertebral spinous process. If the insertion site is too anterior, the lateral cutaneous branch of the intercostal nerve may be missed as it arises at the midaxillary line (see Fig. 31-1). Fluoroscopic guidance is recommended, but not absolutely necessary for performing intercostal nerve blocks. Under sterile conditions, a skin wheal is made with local anesthesia. A 3.5 inch, 25- (or 22-) gauge needle is inserted over the rib and directed perpendicular to the skin. A 15-degree bend away from the bevel of the needle allows the needle to “steer” (bevel is pointing caudad). Longer needles may be needed for obese patients. When the needle contacts the periosteal surface of the inferior portion of the rib bone, it can be rotated 180 degrees, then slowly “walked off ” the rib inferiorly until it just slips off under the rib. The 15-degree bend of the needle tip away from the bevel can facilitate the needle being walked off the rib, with the direction of the bevel cephalad, which then places the bevel of the needle in proximity to the intercostal nerve, (Figs. 31-3 through 31-5) where it is known to lie in the intercostal groove as the classic VAN complex (vein, artery, nerve from cephalad to caudad) (see Fig. 31-2). Another helpful technique is to manually retract the skin superiorly prior to needle insertion, which allows the needle to automatically move inferior when the needle contacts bone. This maneuver reduces needle motion and rotation.2 When the lower rib margin is identified, the needle is then advanced 2 to 3 mm to reach the intercostal groove. After negative aspiration for blood and air, a mixture of 1 to 5 mL of lidocaine or bupivacaine with or without 1: 200,000 epinephrine and/or corticosteroid is injected. The procedure can be repeated in other intercostal segments. Due to collateral innervation, blockade of at least three adjacent segments is often needed to ensure anesthesia/ analgesia in the distribution of the middle intercostal nerve. For a neurolytic intercostal nerve block, sequential injection technique is used to avoid pain induced by neurolytic agents. The inter­costal nerve is first blocked with 3 to 5 mL of 0.5%

bupivacaine with 1: 200,000 epinephrine injected on its proximal site, followed by another injection of a neurolytic agent (e.g., 2 to 3 mL of 100% alcohol) on a site distal to the anesthetized site. To perform a continuous intercostal nerve block, a catheter is placed through a 17-gauge epidural needle. The insertion site is the same as for a single injection, that is, below the lower edge of the rib, close to the posterior axillary line, and 6 to 8 cm lateral to the respective vertebral spinous process. To obtain maximal coverage, the

Figure 31-3  Needle placement in right T12 intercostal groove after “walking off” inferior edge of T12 rib.

Figure 31-5  Washout of contrast along the T12 right intercostal nerve in the intercostal groove.

Figure 31-4  Contrast spread in right T12 intercostal groove.

31

292  Peripheral Nerve Blocks

insertion site should be in the middle of the segments to be blocked. The bevel of the Touhy needle is oriented medially and the tip of epidural catheter is directed medially. After 10 mL of anesthetic solution is injected through the epidural needle, an intercostal catheter is advanced 2 cm and then secured to the skin.3 Appropriate spread of local anesthetics can be confirmed by radiographic imaging with the use of a nonionic contrast agent prior to local anesthetic injection to rule out subarachnoid, intravascular, or pleural placement.

Complications The major complications of an intercostal nerve block are pneumothorax and intravascular injection of local anesthetics. Careful postprocedure monitoring is necessary to detect these complications. The incidence of clinical significant pneumothorax has been reported less than 0.1%.4,5 Careful attention to technique, smallergauge needles, use of fluoroscopic guidance, and avoidance of vigorous needle advancement or probing may help decrease the incidence of this complication. Accidental intravascular injection of local anesthetics during intercostal block is uncommon but potentially serious. It is known that blood levels of local anesthetics after an intercostal nerve block are significantly greater than those after other frequently performed regional anesthetic techniques.6 Adding epinephrine to local anesthetics and aspirating for blood before administering anesthetics, as well as injection of nonionic contrast under continuous fluoroscopy, are important steps that can be taken to minimize intravascular injection of local anesthetics. Other rare complications associated with an intercostal nerve block include infection, hemothorax, hemoptysis, hematoma, tissue necrosis, neuritis, respiratory insufficiency, subarachnoid block, failed block, and allergic reaction to local anesthetics.7 If nonionic contrast is used, anaphylactoid reactions can occur, but are rare, and can be avoided by a pretreatment regimen of prednisone, diphenhydramine, and ranitidine.8

Other Treatments Acute and chronic pain states treated with intercostal nerve block may also be managed with other approaches such as paravertebral block, interpleural block, or thoracic epidural steroid injections, transcutaneous electrical nerve stimulation (TENS), physical therapy, topical anesthetics/NSAIDs, spinal cord stimulation, tricyclic antidepressants, and anticonvulsants.

Conclusion Intercostal nerve block can be a useful intervention for acute and/ or chronic pain in the chest wall. This chapter reviews the block technique with and without image guidance, and describes a safe and effective technique to provide short- and long-term pain relief for a variety of chest wall pain syndromes. REFERENCES 1. Moore KL, Agur AMR. Essential Clinical Anatomy. Philadelphia: Lippincott Williams & Wilkins; 2006. 2. Lennard TA. Pain Procedures in Clinical Practice. Philadelphia: Hanley & Belfus; 2000. 3. O’Kelly E, Garry B. Continuous pain relief for multiple fractured ribs. Br J Anaesth. 1981;53:989-991. 4. Moore DC, Bridenbaugh LD. Intercostal nerve block in 4333 patients: Indications, technique, and complications. Anesth Analg. 1962;41:1-11. 5. Moore DC. Intercostal nerve block for postoperative somatic pain following surgery of thorax and upper abdomen. Br J Anaesth. 1975;47:284-286. 6. Tucker GT, Moore DC, Bridenbaugh PO, et al. Systemic absorption of mepivacaine in commonly used regional block procedures. ­Anesthesiology. 1972;37:277-287. 7. Hidalgo NRA, Ferrante FM. Complications of paravertebral, intercostal nerve blocks and interpleural analgesia. In: Finucane BT, ed. ­Complications of Regional Anesthesia. New York: Springer; 2007. 8. Maddox TG. Adverse reactions to contrast material: Recognition, prevention, and treatment. Am Fam Physician. 2002;66(7):1229-1234.

Supraorbital Nerve Block for Supraorbital Neuralgia

32

Fereshteh Sharonah Soumekh, MD

Anatomy The supraorbital nerve (SON) is purely a general sensory (afferent) nerve. The supraorbital nerve is a continuation of the frontal nerve, which is one of the three main branches of the ophthalmic division (V1) of the trigeminal nerve (the fifth cranial nerve) (Figs. 32-1 and 32-2). The supraorbital nerve exits from the supraorbital foramen or notch along the superior rim of the frontal bone, accompanied by the supraorbital artery. In the supraorbital notch, the supraorbital nerve gives off small filaments that supply the mucosal membrane of the frontal sinus and filaments that supply the upper eyelid. The supraorbital nerve is usually located 2.7 cm from the midline (Fig. 32-3).1,2 The supraorbital nerve course beyond the supraorbital notch has only recently been explored due to advancement in plastic surgical techniques. The detailed anatomic course and its innervations is studied in fresh cadaver specimens and its sensory distribution in living subjects using selective nerve block. SON divides to two branches above the orbital rim, the superficial and deep branches. The medial (superficial) division passes over the frontalis muscle and divides into multiple smaller branches with cephalic distribution toward the hairline. It provides sensory innervations to the forehead skin and anterior scalp as far as the vertex. The deep (lateral) division runs deep in the frontalis across the lateral forehead between the galea aponeurotica and the pericranium. The deep division supplies sensory innervation to underlying periosteum and frontal parietal scalp.3,4 The supratrochlear nerve (STN) is a branch of the frontal nerve and supplies sensory innervations to the bridge of the nose, medial part of the upper eyelid, and medial forehead. The supratrochlear nerve is usually located 1.7 cm from the midline.1,4

Pathophysiology of Supraorbital Neuralgia The supraorbital nerve can be affected by trauma, inflammatory processes, infection, and tumors. Traumatic injuries to skull or soft tissue at the forehead can cause partial or total nerve injuries. This causes numbness and paresthesias in the forehead and anterior skull area. Neoplastic processes can directly or indirectly compromise the supraorbital nerve along its course. Trigeminal neuralgia (tic douloureux) mainly affects the second and third divisions of the trigeminal nerve. The first division

and its branches, including the supraorbital nerve, are affected in about 5% of patients. In most cases, compression by an overlying vein or artery can cause demyelination of the central nervous system portion of the trigeminal nerve. The other causes are demyelinating processes (such as multiple sclerosis) within either the central or peripheral course of the nerve or in the brainstem. Postherpetic neuralgia (PHN) is due to reactivation of the varicella-zoster virus in advanced age, immunocompromised patients, and malignancies such as lymphoma. When the trigeminal nerve is involved, the first division is most commonly affected. After chickenpox has resolved, the virus remains latent in the dorsal root ganglia where it can reactivate later in life. Postherpetic neuralgia is characterized by the persistence of neuropathic pain after the rash has resolved. The pathophysiology of postherpetic neuralgia is unclear; there is evidence of neuronal pathology, peripheral and central demyelination.

Indications Local anesthetics with or without addition of a corticosteroid are used for neural blockade for treatment of pain and neurologic symptoms, based on the following principles: Local anesthetics prevent or relieve pain by interrupting nerve conduction by binding to Na+ channels and blocking their movement, thereby preventing or reducing the activation of action potentials. Steroids inhibit the activation of phospholipase A2 which frees arachidonic acid, the essential substrate for cyclooxygenase and the inflammatory process. Supraorbital nerve blockade has been used routinely alone or in combination with occipital nerve block in a variety of cosmetic, ophthalmologic, and cranial procedures.5 It can be used in chronic pain states that are related to postherpetic neuralgia and supraorbital neuropathy or neuralgias as adjuvant therapy along with pharmacologic treatment or alone. There are several potential sites for supraorbital nerve entrapment, such as a fibrous band at the supraorbital notch and/or compression of the nerve as it travels through muscles or fascia. Supraorbital nerve block has also been used to control pain in intractable headaches. Although the effect of each block is limited in duration, a series of injections appears to provide sustained relief. However, no controlled studies have indicated blocks as a tenable intervention.6 293

294  Peripheral Nerve Blocks

Ophthalmic

Maxillary

Mandibular

Supratrochlear Supraorbital Infratrochlear External nasal Lacrimal

V1

Zygomaticotemporal Zygomaticofacial Infraorbital

V2

Auriculotemporal Buccal Mental

V3

Figure 32-1  Nerve supply for the face (right) and the sensory distribution of the trigeminal nerve (left). (Adapted from NYSORA.com.)

Trigeminal nerve

Trigeminal (gasserian) ganglion

Maxillary nerve (V2)

Ophthalmic nerve (V1)

Mandibular nerve (V3)

Lacrimal nerve

Nasociliary nerve

Frontal nerve

Supratrochlear nerve

Supraorbital nerve

Medial or superficial branch

Lateral or deep branch

Figure 32-2  Anatomy/branches of the trigeminal nerve.

Contraindications to nerve block include the following: infection or hematoma at the puncture site and surrounding area; patient refusal to undergo the procedure; and coagulopathy.

Technique for Nerve Block Patient Position: Supine with head rested on a pillow Bony Landmarks: Superior rim of the frontal bone Soft tissue landmark: Eyebrow

Needle insertion for chronic pain syndromes This diagnostic technique blocks the medial and lateral branches of SON, which supply the forehead and scalp. Insert a 25-gauge

1½ inch needle through the skin about 2 cm above the eyebrow and 2.2 cm from midline. The needle is advanced about 1 inch laterally to 10 o’clock to block the deep (lateral branch) with 1 mL of 1% lidocaine. Then withdraw the needle to insertion point and redirect medially to 12 and 2 o’clock to block the superficial (medial) branch with 1 mL of 1% lidocaine after negative aspiration. There may be resistance during the injection if the needle is located in fascia. This can be avoided by advancing the needle at its entire length and injecting while withdrawing the needle to insertion point. A “fan” technique is recommended to block supraorbital dermatome because of individual variation in the anatomy.7,8 The patient will report numbness of the forehead and vertex in a few minutes if the block is successful. If a diagnostic block is positive and patient reports numbness and relief of pain symptoms

Supraorbital Nerve Block for Supraorbital Neuralgia  295

V1

SON-S

TBr

D

N-

SO

CS STL

TL Syringes

V2

V3 Figure 32-4  Supraorbital nerve block. Figure 32-3  Anatomy of supraorbital nerve. The diagram illustrates the courses of the deep (SON-D) and the superficial (SON-S) divisions of the supraorbital nerve trunk that form just after the trunk exits the supraorbital rim. The SON-D runs superiorly and obliquely across the forehead between the galea aponeurotica and the periosteum by the mid-forehead level, runs parallel to and between 0.5 and 1.5 cm medial to the superior temporal line (STL) of the skull. This relationship with the STL over the forehead continues onto the scalp area. Just before reaching the level of the coronal suture (CS), the SON-D typically bifurcates before forming the fine terminal branches (TBr) that pierce the galea aponeurotica and enter the frontoparietal scalp. The SON-S division forms branches that pass through the lower frontalis muscle at variable levels to run cephalad over this muscle and enter the   anterior scalp. (Adapted from Knize DM: A study of the supraorbital nerve. Plast Reconstr Surg. 1995;96:564-569.)

in the supraorbital nerve distribution, then subsequent block can proceed with corticosteroid injection of 10 to 20 mg of triamcinolone or methylprednisolone, or these can be mixed with the local anesthetic at the time of the block to a 50:50 mixture with local anesthetic with the goal of approximately 1 mL of volume delivered to each of the lateral and medial branches of the supraorbital nerve (Fig. 32-4).

Complications Pain associated with needle insertion is the most commonly reported side effect. Skin elevation or a lump is expected due to the injection of 1 to 2 mL of fluid in a very restricted area. The patient should be reassured that the lump is “injected material” and that this does not represent bleeding or infection. The medication will be absorbed in 24 to 48 hours. Acute shooting pain in the distribution of the nerve is indicative of intraneural injection. The injection should be stopped and the needle should be redirected because injection of solution intraneurally can cause permanent nerve damage. There is a potential risk of infection and hematoma in the vicinity of the puncture site. In the event of hematoma, direct pressure should be applied with the site elevated for 5 to 15 minutes. Infection usually does not manifest until 48 to 72 hours after the injection but may require antibiotics and/or surgical débridement. Repeat nerve blocks with corticosteroids can cause localized lipodystrophy and skin indentation. This can be avoided by use of a fan technique during injection. In the event of neural damage, there is no associated motor paralysis because the supraorbital nerve is a sensory nerve.

Other Treatments for Supraorbital Neuralgia Lidocaine in the form of topical 5% or as a patch has been used for control of postherpetic neuralgia, and may be helpful for supraorbital neuralgia.9 Capsaicin was effective in trials of patients with severe refractory postherpetic neuralgia, however, topical capsaicin products have the risk of eye infiltration and eye damage.10 Oral pharmacologic treatments, tricyclic antidepressants, anticonvulsants, oxycodone, tramadol, dextromethorphan, memantine, mexiletine, and newer drugs such as duloxetine and pregabalin have a role in treatment of postherpetic neuralgia and entrapment neuropathies involving the supraorbital nerve.11-14 Side effects are a limiting factor, especially in the geriatric population and in oncology patients. Surgical resection of forehead muscles as the glabella and ­procerus has been used for control of headaches and may have a role.15 Peripheral nerve stimulation was also shown to be effective in limited case reports.16 REFERENCES   1. Williams PL, Warwick R, Dyson M, Bannister LH, eds. Gray’s Anatomy. 37th ed. London: Churchill Livingstone; 1989:1100.   2. Ramirez OM, Robertson KM. Update in endoscopic forehead rejuvenation. Facial Plast Surg Clin North Am. 2002;10(1):37–51.   3. Knize DM. A study of the supraorbital nerve. Plast Reconstr Surg. 1995;96:564-569.   4. Janis JE, Ghavami A, Lemmon JA, et al. The anatomy of the corrugator supercilii muscle: Part II. Supraorbital nerve branching patterns. Plast Reconstr Surg. 2008;121(1):233-240.   5. Nguyen A, Girard D, Boudreault D, et al. Scalp nerve blocks decrease the severity of pain after craniotomy. Anesth Analg. 2001;93:1272-1276.   6. Bogduk N. Role of anesthesiologic blockade in headache management. Curr Pain Headache Rep. 2004;8(5):399-403.   7. Beer G, Putz R, Mager K, et al. Variations of the frontal exit of the supraorbital nerve: An anatomic study. Plast Reconstr Surg. 1998;102:334-341.   8. Cheng A, Yuen H, Lucas PW, et al. Characterization and localization of the supraorbital and frontal exits of the supraorbital nerve in Chinese: An anatomic study. Ophthal Plast Reconstr Surg. 2006;22(3):209-213.   9. Galer BS, Rowbotham MC, Perander J, Friedman E. Topical lidocaine patch relieves postherpetic neuralgia more effectively than a vehicle topical patch: Results of an enriched enrollment study. Pain. 1999; 80:533-538. 10. Watson CP, Tyler KL, Bickers DR, et al. A randomized vehicle-­ controlled trial of topical capsaicin in the treatment of postherpetic neuralgia. Clin Ther. 1993;15:510-526.

32

296  Peripheral Nerve Blocks 11. Christo PJ, Hobelman G, Maine DN. Post-herpetic neuralgia in older adults: Evidence-based approaches to clinical management. Drugs Aging. 2007;24(1):1-19. 12. Alper BS, Lewis PR. Treatment of postherpetic neuralgia: A systematic review of the literature. J Fam Pract. 2002;51(2):121-128. 13. Dworkin RH, Corbin AE, Young Jr JP, et al. Pregabalin for the ­treatment of postherpetic neuralgia: A randomized, placebo-controlled trial. ­Neurology. 2003;22:60(8):1274–1283.

14. Lewith GT, Field J, Machin D. Acupuncture compared with placebo in postherpetic pain. Pain. 1983;17:361-368. 15. Caputi CA. Firetto V: Therapeutic blockade of greater occipital and supraorbital nerves in migraine patients. Headache. 1997;37(3):174-179. 16. Amin S, Buvanendran A, Park KS, et al. Peripheral nerve stimulator for the treatment of supraorbital neuralgia: A retrospective case series. ­Cephalalgia. 2008;28(4):355-359.

Head and Facial Trigeminal Neuralgia

33

Padma Gulur, MD, Brian J. Wainger, MD, PhD, and Ahn Young, MD

Trigeminal neuralgia is a disease characterized by brief, stereotypical episodes of lancinating pain in the trigeminal nerve distribution on a single side. The vast majority of cases affect either the second or third division (V2 or V3), alone or in combination. In only 4% to 5% of patients, symptoms occur solely in the first division (V1, Table 33-1). Historically, trigeminal neuralgia is considered one of the most painful disorders known to mankind. The name “tic douloureux” was coined by Nicholaus Andre, referring to the spasm of the face that follows an attack of pain. John Fothergill first codified the clinical characteristics of the disease in his paper “On a Painful Affliction of the Face,” which was published in London in 1775. Afflicted patients typically describe the pain as electric, shooting, and shocklike. The pain occurs in attacks, each of which lasts only seconds or less; however, attacks tend to cluster so that painfree episodes may not be appreciated.1,3 Pain can be precipitated by light mechanical stimulation to small trigger zones in the face or oral mucosa. Frequent triggers include light touch, wind, brushing teeth, speaking, eating, and drinking. There may be ipsilateral muscle spasm described in the condition termed tic douloureux. The disease typically takes a sporadic course, with remissions that may last months or even years. Most people have normal neurological examinations and are symptom free between attacks. The annual incidence is between 4 and 5 in 100,000. It typically affects people older than 50 years, although instances of the disease in young adults and even children have been reported. There is a slight female predominance.2 Strong environmental or genetic predisposing factors are not apparent.

Anatomy The disease is thought to result from compression of the trigeminal fibers as they pass from the brainstem to the face. Sites of nerve compression can be divided into brainstem, prepontine, cavernous sinus or Meckel’s cave, and extracranial. Central nervous system causes of trigeminal neuralgia include multiple sclerosis, in which plaques of demyelination can affect exiting pontine fibers. The most frequently affected site is the trigeminal nerve root entry zone—the point at which the transition from central to peripheral myelin occurs. There, tortuous or aberrant vessels can compress the nerve. Indeed, vascular compression is thought to account for 80% to 90% of cases. The nerve then passes into the

prepontine fossa, where it is vulnerable to ectasias of the basilar or vertebral arteries. Tumors of the cerebellopontine angle, as well as arteriovenous malformations, aneurysms, and dural arteriovenous fistulas can all exert pressure on the nerve. After continuing to the apex of the petrous portion of the temporal bone, the nerve traverses the dura to enter Meckel’s cave, a CSF-filled cavity posterolateral to the cavernous sinus, which contains the trigeminal or gasserian ganglion. Infiltrative tumors as well as granulomatous disease can impinge on the ganglion. The nerve then separates into three divisions (Fig. 33-1), each of which can be compressed by local inflammatory conditions or primary neoplastic or metastatic lesions. The ophthalmic nerve (V1) courses anteriorly through the cavernous sinus, where it is accompanied by cranial nerves III, IV, VI, and V.2 It exits the skull through the superior orbital fissure and passes into the orbit. From there, it divides to supply the eyeball, lacrimal glands, conjunctiva, part of the nasal mucosa, and skin of the nose, eyelid, and forehead. The maxillary nerve (V2) also passes through the cavernous sinus and then exits the skull inferolaterally through the foramen rotundum and into the pterygopalatine fossa. The nerve then continues anteriorly in the orbital floor and emerges as the infraorbital nerve, which innervates the middle third of the face and upper teeth. The mandibular nerve (V3) exits the skull more proximally through the foramen ovale and passes into the masticator space. It supplies the lower third of the face as well as the tongue and floor of the mouth and jaw. The motor root, which bypasses the gasserian ganglion but then rejoins the mandibular nerve provides innervation to the muscles of mastication (see Fig. 33-1).

Pathophysiology Although Jannetta and colleagues showed that surgical decompression of the nerve root can effectively alleviate the symptoms of trigeminal neuralgia, a pathophysiologic connection between trigeminal nerve compression and the intermittent nature of the disease has not been well elucidated.4 A disease mechanism must also explain how nonnoxious peripheral mechanical stimuli trigger pain within different regions of the face. In a number of patients who undergo surgical exploration, no compressing vessel or lesion has been identified. 297

298  Peripheral Nerve Blocks

Pathologic rhizotomy specimens have demonstrated focal loss of myelin with close apposition of the demyelinated axons.5,6 Hilton found five patients without microvascular compression who did not show demyelinating features. In the study by Devor and colleagues, 1 of the 12 patients was not found to have vascular compression, and the rhizotomy specimen from this patient showed only “modest dysmyelination”. How the demyelination—if indeed that is not an epiphenomenon—contributes to the pain is also not clear. One possibility is that the compressed and demyelinated neurons may have increased ephaptic transmission, spread from axon to axon versus along an individual axon. Devor and his colleagues proposed their “ignition hypothesis” by which nerve compression leads to an increase in neuronal activity and reduced firing thresholds.6 In support of this hypothesis, Vos and colleagues showed in rats that mild compression of the infraorbital nerve produces a facial pain syndrome.7 There are case reports of bilateral trigeminal neuralgia. Many of these cases result from demyelinating lesions of multiple sclerosis. Other cases have occurred in patients with Charcot-MarieTooth disease, presumably due to an increased sensitivity to nerve compression.

Table 33-1  Distribution of Pain in Trigeminal Neuralgia

Diagnosis The White and Sweet criteria for trigeminal neuralgia8 were a major advance that facilitated research and enabled early and accurate clinical recognition of the syndrome (Tables 33-2 through 33-4). The criteria were incorporated, largely unchanged, into the official research diagnostic framework criteria published by the International Association for the Study of Pain (IASP)9 and the International Headache Society (IHS).3 The current IHS criteria (International Classification of Headache Disorders II [ICHD-II])3 establishes trigeminal neuralgia as a discrete clinical diagnosis under the general classification of “cranial neuralgias and central causes of facial pain” (ICHD-II diagnostic code 13). The diagnosis ‘‘trigeminal neuralgia’’ (diagnostic code 13.1) replaces the earlier term, tic douloureux. ICHD-II further subdivides trigeminal neuralgia into ‘‘classic trigeminal neuralgia’’ and ‘‘symptomatic trigeminal neuralgia.’’ Classic trigeminal neuralgia Table 33-2  Sweet Diagnostic Criteria for Trigeminal Neuralgia 1. The pain is paroxysmal. 2. The pain may be provoked by light touch to the face (trigger zones). 3. The pain is confined to the trigeminal distribution. 4. The pain is unilateral. 5. The clinical sensory examination is normal.

Distribution

%

V1 alone

4

V2 alone

17

V3 alone

15

V2 + V3

32

V1 + V2

14

13.1.1 Classic trigeminal neuralgia:

V1 + V2 + V3

17

A. Paroxysmal attacks of pain lasting from a fraction of a second to   2 minutes, affecting one or more divisions of the trigeminal nerve and fulfilling criteria B and C B. Pain has at least one of the following characteristics: 1. Intense, sharp, superficial, or stabbing 2. Precipitated from trigger areas or by trigger factors C . Attacks are stereotypical in the individual patient D. There is no clinically evident neurological deficit E. Not attributed to another disorder

From White JC, Sweet WH: Pain and the Neurosurgeon. Springfield, Ill. Charles C Thomas, 1969.

Table 33-3  ICHD Criteria for Classic Trigeminal Neuralgia

Gasserian ganglion

Peripheral branches Terminal nerve divisions

Brainstem

ICHD, International Classification of Headache Disorders.

V1 Terminal nerve nucleus

V2 V3

Terminal nerve root Figure 33-1  Anatomy of the trigeminal nerve. Image from http://www.frca. co.uk/images/trigeminal_nerve.jpg, accessed 2010, March 14, courtesy of AnaesthesiaUK.

Table 33-4  ICHD Criteria for Symptomatic Trigeminal Neuralgia 13.1.2 Symptomatic trigeminal neuralgia: A. Paroxysmal attacks of pain lasting from a fraction of a second to   2 minutes, with or without persistence of aching between paroxysms, affecting one or more divisions of the trigeminal nerve and fulfilling criteria B and C B. Pain has at least one of the following characteristics: 1. Intense, sharp, superficial, or stabbing 2. Precipitated from trigger areas or by trigger factors C . Attacks are stereotypical in the individual patient D. A causative lesion, other than vascular compression, has been demonstrated by special investigations and/or posterior fossa exploration ICHD, International Classification of Headache Disorders.

Head and Facial Trigeminal Neuralgia  299

(Table 33-3) is the most common idiopathic form of the disorder (although it also includes cases associated with vascular compression). Classic trigeminal neuralgia is defined as ‘‘a unilateral disorder characterized by brief electric shocklike pains, abrupt in onset and termination, limited to the distribution of one or more divisions of the trigeminal nerve. Pain is commonly evoked by trivial stimuli including washing, shaving, smoking, talking and/or brushing the teeth (trigger factors) and frequently occurs spontaneously. Small areas in the nasolabial fold and/or chin may be particularly susceptible to the precipitation of pain (trigger areas). The pains usually remit for variable periods.’’ The ICHD-II specific diagnostic criteria for classic trigeminal neuralgia are listed in Table 33-3. Symptomatic trigeminal neuralgia has the same key features of trigeminal neuralgia but results from another disease process (such as multiple sclerosis or a cerebellopontine angle tumor). Symptomatic trigeminal neuralgia is defined by IHS as ‘‘Pain indistinguishable from classic trigeminal neuralgia but caused by a demonstrable structural lesion other than vascular compression.’’ The ICHD-II diagnostic criteria for symptomatic trigeminal neuralgia are listed in Table 33-4. Because a significant percentage of patients have symptomatic trigeminal neuralgia resulting from another disease process, diagnostic brain imaging studies should be part of the initial evaluation of any patient with trigeminal neuralgia symptoms.10,11 The study should visualize the anatomic landmarks around the trigeminal (gasserian) ganglion and the cerebellopontine angle. Although a routine brain CT scan is usually adequate to screen for a cerebellopontine tumor, an MRI scan often better demonstrates multiple sclerosis plaques and the anatomic relationships of the trigeminal root. High-resolution imaging techniques are also increasingly able to visualize subtle vascular anomalies that may be the source of root compression in certain patients with classic trigeminal neuralgia. Other diagnostic studies, such as blood studies, lumbar puncture, and evoked potentials, are generally not necessary.

Medical Treatment Carbamazepine has been the mainstay of medical treatment for trigeminal neuralgia for many years.12 A Cochrane review on this subject confirmed that carbamazepine with a number needed to treat (the number of people who would need to be treated to see benefit in one person) of 2.5 was the recommended initial treatment for trigeminal neuralgia.13 Antiepileptic drugs were first used in the treatment of trigeminal neuralgia when Bergouignan in 1942 noted that the anticonvulsant phenytoin effectively controlled attacks of pain in the condition.14 Studies on various antiepileptic drugs have revealed that although carbamazepine and lamotrigine are superior to placebo in trials, most others drugs thought to be useful do not have trials to support their use.15 Baclofen is another choice for monotherapy for trigeminal neuralgia as was evidenced in data from Fromm and colleagues.16 In many instances where carbamazepine is not tolerated, initial therapy with baclofen has been successful. Clonazepam is a benzodiazepine with anticonvulsant properties and is also effective for suppression of pain attacks. Gabapentin, topiramate, oxcarbazepine, tiagabine, levetiracetam, and zonisamide have also been effective in treatment of trigeminal neuralgia, although the number of published clinical studies with these agents is presently small.

Therapy routinely begins with one agent, given in gradually increasing doses until pain attacks are suppressed or reduced in intensity. When a patient only partially responds to single-drug therapy at dosages that evoke side effects, rotation to another agent or adding a second drug may enhance the therapeutic response. Although the drugs are classified as anticonvulsants, they have differing mechanisms of action as well as side effect patterns. In a retrospective study of anticonvulsant therapy, Scrivani and coworkers found that 50% of patients reported satisfactory pain relief while taking a single antiepileptic drug, whereas 70% of those taking two drugs reported a satisfactory response.17

Interventional Approaches These can be broadly classified as peripheral techniques and those directed at the gasserian ganglion. In general, when surgical options are considered, techniques directed at the gasserian ganglion have largely replaced peripheral techniques. We will also approach neurostimulation and its role in the management of trigeminal neuralgia. There is a paucity in the literature directly comparing medical management with surgical management. Given inconsistency in outcome measurements, poor quality of studies (most do not have independent assessment), and lack of direct comparisons, this leads to a limited ability to truly assess. Zakrzewska and associates compared the medical and surgical management of intractable trigeminal neuralgia. This is a long-term prospective longitudinal study comparing 15 patients who were followed for a mean duration of 15 years on the effectiveness of medical (oxcarbazepine) versus surgical therapy. The study indicated that mean time to recurrence of pain following oxcarbazepine therapy was 8 months and with surgical therapy it was 28 months. Clinical and patient global analysis of the outcome measures suggested that patients could benefit substantially from having surgery earlier, rather than later, in the disease process to improve the quality of life, freedom from medication, and the need for regular follow-up. Remember: this was a study group of only 15 patients.19

Peripheral Nerve Blocks Peripheral nerve ablation is a procedure that locally blocks the division of the trigeminal nerve involved with pain. The means of ablation typically include local (peripheral) blocks with local anesthetics, neurectomy of the involved trigeminal branch under local anesthesia, cryotherapy or neurolytic blocks with alcohol or phenol. For all the listed blocks, consider the addition of a small amount of corticosteroid for therapeutic purposes.

Block of the Ophthalmic Nerve The ophthalmic nerve per se is not blocked in the treatment of trigeminal neuralgia because it leads to keratitis. The supraorbital and supratrochlear branches can be individually blocked. The supraorbital nerve block is described elsewhere in this text. The supratrochlear nerve can be injected at the superior medial corner of the orbital ridge with 1 mL of local anesthetic with or without corticosteroid. The inferior orbital nerve can be injected at the inferior orbital foramen which is 1 cm below the orbit and is usually located with a needle inserted about 2 cm lateral to the

33

300  Peripheral Nerve Blocks

Supraorbital nerve block

Supratrochlear nerve block

Maxillary Semilunar ganglion

3

Infratrochlear nerve block

1 2

Mandibular

A Infraorbital nerve block Maxillary Figure 33-2  Supraorbital, supratrochlear, infratrochlear, and infraorbital nerve blocks.

Semilunar ganglion

nasal and directed superiorly, posteriorly, and slightly laterally (Fig. 33-2).

3

Block of the Maxillary Nerve and Its Branches With the patient’s mouth opened, a 3.5-inch, 25-gauge needle can be inserted between the zygomatic arch and the notch of the mandible. At about 3 to 4 cm in depth, contact will be made with the lateral pterygoid plate. Withdraw the needle 1 cm and angle it superiorly and anteriorly to pass into the pterygopalatine fossa. Local anesthetic (4 to 6 mL) can then be instilled here after negative aspiration. This technique anesthetizes the maxillary nerve and the sphenopalatine ganglion. There is a risk of hemorrhage when blocking the maxillary nerve with this technique (Fig 33-3).

Block of the Mandibular Nerve and Its Branches The mouth is slightly opened and a 25-gauge, 3.5-inch needle is advanced between the zygomatic arch and the mandibular notch. After contact with the lateral pterygoid plate, withdraw the needle one centimeter and angle superior and posterior toward the ear. About 4 to 6 mL of local anesthetic is then instilled at this location after negative aspiration. The facial nerve may at times be unintentionally blocked with this technique. The lingual and inferior mandibular nerves can be injected with the mouth opened and by palpating the coronoid notch. The needle is introduced medial to the notch but lateral to the pterygomandibular fold and advanced posteriorly about 2 cm along the medial aspect of the mandibular ramus where 2 to 3 mL of local anesthetic, when instilled, will block both nerves. The inferior alveolar nerve is blocked as it emerges from the mental foramen at mid-mandible 2 mL of local anesthetic is instilled when paresthesias are elicited or the needle enters the foramen.

1 2

Mandibular

B Figure 33-3  Maxillary nerve block.

Mandibular Nerve Block Local Anesthetics and Streptomycin Trigeminal nerve blocks with local anesthetics, usually lidocaine, have been described in multiple reports to provide relief but usually are very short lived. A study on intranasal application of lidocaine to the pterygopalatine fossa showed brief improvement in 25 patients with V2 treated with intranasal 8% lidocaine spray compared to placebo; however, the relief lasted only 4 hours on average, with a maximum duration of 24 hours.18 An uncontrolled report using a high concentration of lidocaine for trigeminal nerve blocks documented much longer durations of improvement with many patients obtaining months of pain control.20 Studies looking at the use of streptomycin and lidocaine for trigeminal nerve block have largely shown no significant improvement.21

Neurectomy Neurectomy is probably the oldest recorded surgical procedure for trigeminal neuralgia. Most of the studies done for neurectomy were retrospective and published more than 20 years ago with only one recent paper by Murali and Rovit. They reported on a case series of 40 patients, 12 with neurectomies performed as the primary

Head and Facial Trigeminal Neuralgia  301

33

procedure, and 28 as a secondary procedure to treat pain recurrence after radiofrequency thermocoagulation.22 The follow-up period was 2 to 10 years. It was reported that 79% had excellent pain relief (defined as total loss of pain without need of medication) lasting 5 years or more, and some had excellent pain relief until their deaths. The mean age of their patients was 72 years with an age range of 50 to 94 years. Dysesthesia or sensory loss in the area supplied by the nerve was reported as a significant morbidity of the surgery.

Cryotherapy Cryotherapy is the therapeutic use of extremely low temperatures to destroy cells by crystallizing the cytosol to obtain pain relief. Under local anesthesia, the affected nerve is exposed surgically and a cryoprobe is placed directly on the nerve for three 2-minute freeze-thaw cycles. Few complications have been reported; sensation, although initially lost, returns before pain recurs.23,24 The procedure can be repeated, and the results have been similar.

Neurolytic Peripheral Blocks Neurolytic peripheral blocks of the trigeminal nerve and its branches are usually done with phenol or alcohol. Most studies on these techniques are older retrospective analyses. A more recent paper by Fardy and Patton, reported on a series of 413 alcohol blocks administered over a 20-year period. The mean period of pain relief was 13 months, and only three (0.73%) significant complications were noted.25 These included local tissue necrosis, diplopia, and sensory loss. Disadvantages to this procedure include sensory loss in the distribution of the treated nerve and a high rate of recurrence of pain owing to nerve regeneration with subsequent deafferentation pain.

Figure 33-4  Percutaneous needle to the gasserian ganglion. (Image from ­http://www.umanitoba.ca/cranial_nerves/trigeminal neuralgia/manuscript/ rhizotomies.html; © 2001, The Centre for Cranial Nerve Disorders.)

Trigeminal nerve

Gasserian Ganglion Techniques Techniques targeting the gasserian ganglion can broadly be classified into ablative and decompressive approaches. Percutaneous trigeminal ablation of the gasserian ganglion is usually performed by a specially designed device inserted into the cheek or through the mouth. Under radiographic guidance with fluoroscopy or CT, the device is directed through the foramen ovale into the gasserian ganglion or retrogasserian rootlets. The methods of ablation typically include radiofrequency coagulation, glycerol injection, and mechanotrauma by balloon ablation. The results from any of these modalities depends on the duration and intensity of denervation (Fig. 33-4). Radiofrequency Thermocoagulation Radiofrequency thermocoagulation is the most common surgical treatment for trigeminal neuralgia. A meta-analysis of the literature confirmed the efficacy of this procedure.26 The recurrence rate quoted ranges from 4% to 65%.This wide variation in part was due to differing standards for defining recurrence. Some studies classified recurrence as pain severe enough to require surgery, and others as in recurrence of symptoms. The most important factors influencing recurrence are the duration of follow-up and the degree of denervation. Taha and Tew reviewed the therapy in 500 patients that were followed for 2 to 12 years with patients who had undergone other surgical treatments for trigeminal neuralgia.27 The authors found a 100% technical success rate for completion of the radiofrequency procedure, the highest rates for initial pain relief, and one of the lowest pain recurrence rates for RT (radiofrequency treatment)

1st branch

2nd branch 3rd branch

Radiofrequency Needle Figure 33-5  Radiofrequency lesioning of trigeminal nerve. (Image from http://www.spinesurgeon.com.au/Neurological_Conditions/images/trigeminal_  Neuralgia_clip_image009.jpg, accessed 2010, March 14.)

when compared with other surgical procedures. A recurrence rate of only 20% in 9 years was reported (Fig 33-5). Glycerol Injections Percutaneous injection of glycerol was described initially by Hakanson.28 Glycerol injection involves the injection of sterile glycerol into the gasserian ganglion and retrogasserian rootlets. Placement of the needle adjacent to the ganglion is confirmed with contrast cisternogram. The procedure results in significant initial pain relief.

302  Peripheral Nerve Blocks

North, in 1990, reviewed 109 percutaneous retrogasserian glycerol rhizotomies in 85 patients, 11 with atypical features (constant pain and/or significant sensory loss unexplained by prior procedures).29 They were followed for 6 to 54 months. The endpoints were recurrence requiring medication and recurrence refractory to medication requiring further intervention. Mean duration for primary endpoint was 2 years, and 3 years for secondary endpoint. Mean time to failure of repeat treatment was 1 year. There were two reported cases of corneal anesthesia and three of hyperesthesia. As initially described, there was a low incidence of complications, dysesthesia, or keratitis, and little loss of sensation. In fact, glycerol injection replaced neurolysis by ethanol and phenol, both of which caused significant sensory loss. However, many recent larger series have shown that complications do occur frequently, and the recurrence rate is relatively high, up to 50%.30-32 Balloon Microcompression Balloon microcompression of the trigeminal ganglion is done with a Fogarty balloon catheter that can be inserted under fluoroscopy. This requires the use of a larger needle (14 gauge) from which a catheter is threaded through the foramen ovale. The balloon is inflated to predetermined pressure. This can cause temporary motor loss. There are also reports of bradyarrhythmias and blood pressure variation from the trigeminal cardiac reflex. Fewer studies have been done for this technique compared with radiofrequency thermocoagulation and glycerol injection. Lichtor and colleagues reported a 10-year follow-up in a series of 100 patients. At 5 years, the recurrence rate was 20%, and at 10 years, it is estimated that 70% of patients will still be pain free.33 One of the main advantages of this procedure is that the corneal reflex is maintained in most cases. However, dysesthesia occurs in 7% to 19% of the cases and may be related to compression time. Skirving and coworkers in a retrospective review of balloon compression found there was prompt pain relief in 521/522 patients.34 The recurrence rate was 19.2% within 5 years. There were symptomatic dysesthesias in 3.8% of patients (Fig 33-6).

Figure 33-6  Balloon decompression gasserian ganglion. (Image from http://fns. med.upatras.gr/images/image100.jpg, accessed 2010, March 14; courtesy of Constantine Constantoyannis, MD, Functional Neurosurgery, University of Patras, Greece. © 2008.)

Stereotactic Radiosurgery Stereotactic radiosurgery is becoming more widely practiced and is the least invasive of these procedures. A stereotactic head frame is screwed onto the skull, and stereotactic imaging is performed. The trigeminal system is irradiated. A maximum radiosurgical dose of 70 Gy or greater was associated with a greater chance of complete pain relief. Pain relief begins approximately 3 to 6 months after the procedure. Disadvantages of this technique include a roughly 20% to 30% risk of decreased sensation in the nerve after the treatment. Radiosurgery involves the application of ionizing radiation to a portion of the brain. The long-term effects of targeted radiation to the brain have not been studied. Most patient series enrolled fewer than 100 patients with follow-up of less than 1 year. Kondziolka and associates reported 80% initial pain relief in 106 patients who were followed for 18 months.35 Ten percent of the patients developed dysesthesia as a complication (Fig 33-7).

Decompressive Procedures These procedures are based on the concept that compression of the trigeminal nerve causes trigeminal neuralgia.36 The compression of the trigeminal nerve from blood vessels or tumors is thought to

Figure 33-7  Gamma knife surgery. (Image from http://www.umanitoba.ca/ cranial_nerves/trigeminal_neuralgia/manuscript/rhizotomies.html; © 2001, The Centre for Cranial Nerve Disorders.)

result in demyelination of the nerve. There is evidence from clinical and anatomic studies that supports the neurovascular compression theory of trigeminal neuralgia.37,38 However, there are many patients who do not experience pain relief following ­trigeminal nerve decompression, suggesting that there are etiologies other than compression of the nerve that could cause trigeminal ­neuralgia (Fig 33-8). Microvascular Decompression Microvascular decompression is indicated in patients who are unable to achieve adequate relief through medical management and have an anticipated survival greater than 5 years and are considered candidates for a craniotomy under general anesthesia. Walter Dandy was the first to put forth the posterior fossa approach for the treatment of trigeminal neuralgia.39 In 1934, Dandy proposed his theory of vascular compression as a cause, but also acknowledged that vascular contact occasionally occurs

Head and Facial Trigeminal Neuralgia  303

33 I

Artery

Trigeminal nerve

II V

Pad III

VII VI

VIII IX X XI

IV

XII Tentorium

Figure 33-8  Posterior fossa with trigeminal nerve (V) shown. (Image from http://www.mayfieldclinic.com/PE-AnatBrain.htm, accessed 2010, March 14; © Mayfield Clinic.)

without the production of pain and may be absent when neuralgia is present. Dandy identified the major compressing vessel as the anterior inferior cerebellar artery. Peter Jannetta documented the frequent occurrence of vascular channels compressing the trigeminal nerve in patients with trigeminal neuralgia and devised a technique for nondestructive microvascular decompression of the nerve.40 Microvascular decompression involves a craniotomy to expose the nerve at the base of the brainstem and to then insert a tiny polytetrafluoroethylene (Teflon) pad between the compressing vessel and the nerve. This Teflon pad isolates the nerve from the pulsating effect and pressure of the blood vessel. Barker and colleagues have reported an excellent long-term (20 years) prospective longitudinal study on the outcome of microvascular decompression for trigeminal neuralgia in 1185 patients. Ten years after surgery, 70% of the patients had excellent final results; they were free of pain without need for medication. Major complications included deaths (0.2%), brainstem infarction (0.1%), and ipsilateral hearing loss (1%). Initial relief of neuralgia pain was present in 98% of patients41 (Fig. 33-9).

Neurostimulation for Trigeminal Neuralgia Neuromodulation in the treatment of trigeminal neuralgia has been studied in multiple ways. Deep brain stimulation of well-defined targets in the sensory thalamus and periaqueductal or periventricular gray matter with stereotactic placement of electrodes has been studied but has not proven to be efficacious.42 Motor cortex stimulation on the other hand needs further evaluation with well designed studies but early reports have been promising in the treatment of intractable cases. The procedure involves stimulation of the motor cortex by an epidural lead. Preoperatively the precentral gyrus is located by electrode recording using three-dimensional magnetic resonance imaging

Figure 33-9  Microvascular decompression. (Image from http://www. health-res.com/EX/07-27-22/ph.mvdsurgery.gif, accessed 2010, March 14.)

of the brain surface with a reference grid attached to the patient’s skin or by a stereotactic frame-based MRI. Operatively, usually under general anesthesia, a craniotomy is performed and a quadripolar plate electrode is inserted into the epidural space, above the precentral gyrus. The facial motor region is stimulated using the grid electrode and the face is observed for indications of muscular contraction. Intraoperative electrode stimulation may result in complete pain relief. A longer trial stimulation is usually performed before permanent implantation of a pulse generator. In a few studies, excellent results have been documented in the treatment of trigeminal neuropathic pain, with 75% to 100% of patients achieving good or excellent pain relief.43-45 The effect of motor cortex stimulation can wane over time, requiring reprogramming. Even in patients who undergo intensive reprogramming, pain relief cannot always be achieved.46 Although the development of epilepsy has not been reported, there is a risk of seizures during stimulator programming. In summary, of the neuromodulatory techniques, motor cortex stimulation shows some early promise.

Conclusion Trigeminal neuralgia is estimated to affect 1 in 15,000 people. Diagnosis especially with atypical presentations can be challenging and diagnostic nerve blocks as described earlier can be helpful. Although the mainstay of therapy is still medications, neurolysis, surgical options, and neuromodulation have all been employed to treat advanced presentations. REFERENCES   1. Katusic S, Williams DB, Beard CM, et al. Epidemiology and clinical features of idiopathic trigeminal neuralgia and glossopharyngeal neuralgia: similarities and differences, Rochester, Minnesota, 1945-1984. Neurepidemiology. 1991;10:276-281.   2. Katusic S, Beard CM, Bergstralh E, Kurland LT. Incidence and clinical features of trigeminal neuralgia. Rochester, Minnesota, 1945-1984. Ann Neurol. 1990;27(1):89-95.   3. Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders. 2nd ed. Cephalalgia. 2004;24(suppl 1):9-160.   4. Jannetta PJ. Neurovascular compression in cranial nerve and systemic disease. Ann Surg. 1980;192(4):518-525.

304  Peripheral Nerve Blocks   5. Hilton DA, Love S, Gradidge T, Coakham HB. Pathological findings associated with trigeminal neuralgia caused by vascular compression. Neurosurgery. 1994;35(2):299-303.   6. Devor M, Amir R, Rappaport ZH. Pathophysiology of trigeminal neuralgia: The ignition hypothesis. Clin J Pain. 2002;18:4-13.   7. Vos BP, Strassman AM, Maciewicz RJ, et al. Behavioral evidence of trigeminal neuropathic pain following loose constrictive ligation of the rat’s infraorbital nerve. J Neurosci. 1994;14:2708-2723.   8. White JC, Sweet WH. Pain and the Neurosurgeon. Springfield, Ill: Charles C Thomas; 1969.   9. Merskey H, Bogduk N. Classification of chronic pain: Descriptions of chronic pain syndromes and definitions of pain terms. IASP Press; 1994. 10. Vitte E, Bensimon JL, Baulac M. Radiological studies in trigeminal nerve pathology. Arch Otorhinolaryngol. 1989;246:262-264. 11. Yang J, Simonson TM, Ruprecht A, et al. Magnetic resonance imaging used to assess patients with trigeminal neuralgia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996;81:343-350. 12. McQuay H, Carroll D, Jadad AR, et al. Anticonvulsant drugs for management of pain: A systematic review. BMJ. 1995;311(7012):1047-1052. 13. Wiffen PJ, McQuay HJ, Moore RA. Carbamazepine for acute and chronic pain. Cochrane Database Syst Rev. 2005;(3):CD005451. 14. Bergouignan M. Cures heureuses de ne´vralgies facials essentielles par le diphe´nylhydantoinate de soude. Rev Laryng (Bordeaux). 1942;63:34-41. 15. Sindrup SH, Jensen TS. Pharmacotherapy of trigeminal neuralgia. Clin J Pain. 2002;18:22-27. 16. Fromm GH, Terrence CF, Chattha AS. Baclofen in the treatment of trigeminal neuralgia: Double-blind study and long-term follow-up. Ann Neurol. 1984;15(3):240-244. 17. Scrivani SJ, Mathews ES, Maciewics RJ. Trigeminal neuralgia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2005;100:527-538. 18. Kanai A, Suzuki A, Kobayashi M, Hoka S. Intranasal lidocaine 8% spray for second-division trigeminal neuralgia. Br J Anaesth. 2006;97: 559-563. 19. Zakrzewska JM, Patsalos PN. Long-term cohort study comparing medical (oxcarbazepine) and surgical management of intractable trigeminal neuralgia. Pain. 2002;95:259-266. 20. Han KR, Kim C, Chae YJ, Kim DW. Efficacy and safety of high concentration lidocaine for trigeminal nerve block in patients with trigeminal neuralgia. Int J Clin Pract. 2008;62:248-254. 21. Bittar GT, Graff-Radford SB. The effects of streptomycin/lidocaine block on trigeminal neuralgia: A double blind crossover placebo controlled study. Headache. 1993;33:155-160. 22. Murali R, Rovit RL. Are peripheral neurectomies of value in the treatment of trigeminal neuralgia? An analysis of new cases and cases involving previous radiofrequency gasserian thermocoagulation. J Neurosurg. 1996;85:435-437. 23. Zakrzewska JM, Nally FF. The role of cryotherapy (cryoanalgesia) in the management of paroxysmal trigeminal neuralgia: A six year experience. Br J Oral Maxillofac Surg. 1988;26:18-25. 24. Zakrzewska JM. Cryotherapy for trigeminal neuralgia: A 10 year audit. Br J Oral Maxillofac Surg. 1991;29:1-4. 25. Fardy MJ, Patton DW. Complications associated with peripheral alcohol injections in the management of trigeminal neuralgia. Br J Oral Maxillofac Surg. 1994;32:387-391.

26. Zakrzewska JM. Trigeminal Neuralgia. London: WB Saunders; 1995: 125-156. 27. Taha JM, Tew JM. Comparison of surgical treatments for trigeminal neuralgia: Evaluation of radiofrequency rhizotomy. Neurosurg. 1996;38:865-871. 28. Hakanson S. Trigeminal neuralgia treated by the injection of glycerol into the trigeminal cistern. Neurosurgery. 1981;9:638-646. 29. North RB, Kidd DH, Piantadosi S, Carson BS. Percutaneous retrogasserian glycerol rhizotomy. Predictors of success and failure in treatment of trigeminal neuralgia. J Neurosurg. 1990;72:851-856. 30. Burchiel KJ. Percutaneous retrogasserian glycerol rhizolysis in the management of trigeminal neuralgia. J Neurosurg. 1988;69:361-366. 31. Saini SS. Retrogasserian glycerol injection therapy in trigeminal neuralgia. J Neurol Neurosurg Psych. 1987;50:1536-1538. 32. Fujimiki T, Fukushima T, Miyazaki S. Percutaneous retrogasserian glycerol injection in the management of trigeminal neuralgia: Long-term follow-up results. J Neurosurg. 1990;3:212-216. 33. Lichtor T, Mullan JF. A 10-year follow-up review of percutaneous microcompression of the trigeminal ganglion. J Neurosurg. 1990;72:49-54. 34. Skirving DJ, Dan NG. A 20-year review of percutaneous balloon compression of the trigeminal ganglion. J Neurosurg. 2001;94(6):913-917. 35. Kondziolka D, Lunsford LD, Flickinger JC. Stereotactic radiosurgery for the treatment of trigeminal neuralgia. Clin J Pain. 2002;18:42-47. 36. Jannetta PJ. Treatment of trigeminal neuralgia by suboccipital and transtentorial cranial operations. Clin Neurosurg. 1977;24:538-549. 37. Hamilyn PJ, King TT. Neurovascular compression in trigeminal neuralgia: A clinical and anatomical study. J Neurosurg. 1992;76:948-954. 38. Devor M, Lippman RG, Rappaport ZH. Mechanism of trigeminal neuralgia: An ultrastructural analysis of trigeminal root specimens obtained during microvascular decompression surgery. J Neurosurg. 2002;96:532-543. 39. Dandy WE. Concerning the cause of trigeminal neuralgia. Am J Surg. 1934;24:447-455. 40. Jannetta PJ. Microvascular decompression of the trigeminal nerve for tic douloreux. In: winn RH, ed. Youmans—Neurological Surgery. 4th ed. Philadelphia: Saunders; 1996:3404-3415. 41. Barker FG 2nd, Jannetta PJ, Bissoneete DJ, et al. The long-term outcome of microvascular decompression for trigeminal neuralgia. N Eng J Med. 1996;334:1077-1083. 42. Coffey RJ. Deep brain stimulation for chronic pain: Results of two multicenter trials and a structured review. Pain Med. 2001;2:183-192. 43. Meyerson BA, Lindblom U, Linderoth B, et al. Motor cortex stimulation as treatment of trigeminal neuropathic pain. Acta Neurochir Suppl (Wien). 1993;58:150-153. 44. Ebel H, Rust D, Tronnier V, et al. Chronic precentral stimulation in trigeminal neuropathic pain. Acta Neurochir (Wien). 1996;138:1300-1306. 45. Rainov NG, Fels C, Heidecke V, Burkert W. Epidural electrical stimulation of the motor cortex in patients with facial neuralgia. Clin Neurol Neurosurg. 1997;99:205-209. 46. Henderson JM, Boongird A, Rosenow JM, et al. Recovery of pain control by intensive reprogramming after loss of benefit from motor cortex stimulation for neuropathic pain. Stereotact Funct Neurosurg. 2004;82:207-213.

34

Occipital Neuralgia* Aneesh K. Singla, MD, MPH, and Julie K. Silver, MD

Anatomy Occipital neuralgia is one type of cervicogenic headache described as pain in the distribution of the greater and/or lesser occipital nerve(s), associated with posterior scalp dysesthesia and/or hyperalgesia. The greater occipital nerve innervates the posterior skull from the suboccipital area to the vertex. It is formed from the medial (sensory) branch of the posterior division of the second cervical nerve.1 It emerges between the atlas and lamina of the axis below the oblique inferior muscle and then ascends obliquely on the latter muscle between it and the semispinalis muscle.1 The course of the greater occipital nerve does not appear to differ in males and females.2 The lesser occipital nerve forms from the medial (sensory) branch of the posterior division of the third cervical nerve, ascends similar to the greater occipital nerve, and pierces the splenius capitis and trapezius muscles just medial to the greater occipital nerve.1,2 It ascends along the scalp to reach the vertex, where it provides sensory fibers to the area of the scalp lateral to the greater occipital nerve. The Occipital neuralgia (for clarity) appears to be more common in females.3

Symptoms Occipital neuralgia may occur as an intermittent (paroxysmal) or a continuous headache. In continuous occipital neuralgia, the headaches may be further classified as acute or chronic. Paroxysmal occipital neuralgia describes pain occurring only in the distribution of the greater occipital nerve. The attacks are unilateral, and the pain is sudden and severe. The pain is described as a lancinating, sharp, throbbing, electric shock-like pain.4-6 The pain may demonstrate a burning characteristic, but this is less common. Although single flashes of pain may occur, multiple attacks are more frequent. The attacks may occur spontaneously or be provoked by specific maneuvers applied to the back of the scalp or neck regions, such as brushing the hair or moving the neck.7 Two broad categories of patients with occipital neuralgia are those with structural pathology and those without apparent etiology.1 Proposed etiologies include myofascial tightening, trauma of C2 nerve root (whiplash injury), prior skull or suboccipital surgery, other type of nerve entrapment, idiopathic causes, hypertrophied atlantoepistrophic *This chapter was adapted with permission from the Essentials of Physical Medicine and Rehabilitation. (Singla A. Occipital Neuralgia. In Fontera WR, Silver JK, Rizzo TD. Essentials of Physical Medicine and Rehabilitation. 2nd ed. Philadelphia, Saunders, 2008, 483-490.)

(C1-2) ligament, sustained neck muscle contractions, or spondylosis of the cervical facet joints (particularly C2-3 and C3-4).4,6,8-11 Most patients with occipital neuralgia do not have discernible lesions.1 Acute continuous occipital neuralgia often has an underlying etiology. The attacks last for many hours and are typically devoid of radiating symptoms (e.g., trigger zones to the face). The entire episode of neuralgia will continue up to 2 weeks before remission. Exposure to cold is a common trigger.7 In chronic continuous occipital neuralgia, the patient may experience painful attacks that last for days to weeks. These attacks are generally accompanied by localized spasm of the cervical or occipital muscles. The reported pain originates in the suboccipital region up to the vertex and radiates to the frontotemporal region. Radiation to the orbital region is also common. Sensory triggers to the face or skull can initiate a painful episode. Similarly, pain may increase with pressure of the head on a pillow. Prolonged abnormal fixed postures that occur in reading or sleeping positions and hyperextension or rotation of the head to the involved side may provoke the pain. The pain may be bilateral, although the unilateral pattern is more common. Often, a previous history of cervical or occipital trauma or arthritic disease of the cervical spine is obtained. Occasionally, patients may report other autonomic symptoms concurrently such as nausea, vomiting, photophobia, diplopia, ocular and nasal congestion, tinnitus, and vertigo.7 Severe ocular pain has also been described, as well as symptoms in other distributions of the trigeminal nerve.8,12-14 Convergence of sensory input from the upper cervical nerve roots into the trigeminal nucleus may explain this phenomenon.11 On examination, pain is sometimes reproduced by palpation of the greater and/or lesser occipital nerves. Tinel’s sign may be present by performing this over the occipital nerves at the subocciput or superior nuchal line. Allodynia and/or hyperalgesia may be present in the nerve distribution. Myofascial pain may be present in the neck or shoulders. Pain may limit cervical range of motion. Neurologic examination of the head, neck, and upper extremities is generally normal. Entrapment of the nerve near the cervical spine may result in increased symptoms during flexion, extension, or rotation of the head and neck. Compression of the skull on the neck (Spurling’s maneuver), especially with extension and rotation of the neck to the affected side, may reproduce or increase the patient’s pain if cervical degenerative disease is the cause of the neuralgia.7 Pressure over both the occipital nerves along their course in the neck and occiput, or pressure on the C2-3 or C3-4 facet joints should cause an exacerbation of pain in such patients, at least when the headache is present. Even if the actual pathology is in the cervical spine, tenderness over the occipital nerve at the superior nuchal line is usually present. 305

306  Peripheral Nerve Blocks

Sensory distribution of greater occipital nerve Sensory distribution of lesser occipital nerve

Greater occipital nerve

Superior nuchal ridge

Occipital artery

Tendinous arch

Mastoid process Figure 34-1  Occipital nerve anatomy. The greater occipital nerve pierces the fascia just below the superior nuchal ridge along with the artery. It supplies the medial portion of the posterior scalp. The lesser occipital nerve passes superiorly along the posterior border of the sternocleidomastoid muscle, dividing into the cutaneous branches that innervate the lateral portion of the posterior scalp and the cranial surface of the pinna. (From Waldman SD: Greater and lesser occipital nerve block. In Waldman SD (ed): Atlas of Interventional Pain Management, 2nd ed. Philadelphia, Saunders, 2004, pp 23-26.)29

The diagnosis of occipital neuralgia is generally made clinically, based on history and physical examination. Imaging may help confirm the diagnosis when there is an anatomic cause such as cervical spondylosis. Diagnostic local anesthetic nerve blocks may be required to obtain a definitive diagnosis; these blocks are done with or without the addition of corticosteroid.1,4,11 The relief of pain after a diagnostic local anesthetic block of the greater/lesser occipital nerves is generally confirmatory of the diagnosis of occipital neuralgia.

Indications for Nerve Block Appropriate treatment interventions for pain from occipital neuralgia may include oral medications, heat/cold therapy, massage, avoidance of excessive cervical spine flexion/extension or rotation, acupuncture, application of transcutaneous electrical nerve stimulation (TENS), physical therapy, nerve block and—in rare cases— neuromodulation/nerve stimulators or surgery.15-19 Blockade of the greater or lesser occipital nerve with a local anesthetic is diagnostic and therapeutic (Fig. 34-2). Pain relief can vary from hours to months. In general, at least 50% of patients will experience more than 1 week of relief after one injection. Case reports of isolated pain relief for greater than 17 months have been achieved after a series of five blocks.6 The addition of a corticosteroid preparation is controversial, but it may provide additional benefit.3

Lesser occipital nerve

Sternocleidomastoid muscle

Trapezius muscle

Splenius capitis muscle

Figure 34-2  Corticosteroid/anesthetic nerve block. The patient is placed in a sitting position with the cervical spine flexed and the forehead on a padded bedside table. A total of 8 mL of local anesthetic is drawn up in a 12 mL sterile syringe. A total of 80 mg of depot-steroid is added to the local anesthetic with the first block and 40 mg with subsequent blocks. The occipital artery is palpated at the level of the superior nuchal ridge. After preparation of the skin with antiseptic solution, a 22 or 25 gauge, 1.5-inch needle is inserted just medial to the artery and is advanced perpendicularly until the needle approaches the periosteum of the underlying occipital bone. A paresthesia may be encountered. The needle is then redirected superiorly, and after   gentle aspiration 5 mL of solution is injected in a fanlike distribution with care being taken to avoid the foramen magnum. (From Waldman SD: Greater and lesser occipital nerve block. In Waldman SD (ed): Atlas of Interventional Pain Management, 2nd ed. Philadelphia, Saunders, 2004, pp 23-26.)29 Botulinum toxin block. The same procedure is used with 50-150 units of botulinum toxin A.30 (From Kapural L, Stillman M, Kapural M, et al: Botulinum toxin occipital nerve block for the treatment of severe occipital neuralgia:   A case series. Pain Pract. 7:337-340, 2007.)

Occipital Neuralgia  307 Anterior

Posterior

SCM

TM LS SM

4 TR C3

1 3

2

C3

Figure 34-3  Ultrasound image transversal view (TV) of the C2-C3 zygapophysial joint. The gray circle indicates the target point for the needle tip during the ultrasound-guided needle placement for third occipital nerve block. 1, C2-3 joint line; 2, Superior articular process of C3; 3, Inferior articular process of C2; 4, Intervertebral foramen of C2-3; C3, white reflex of the surface of the vertebral body of C3; LS = Levator scapulae muscle; SCM, Sternocleidomastoid muscle; SM, Scalenus medius muscle; TM, Trapezius muscle; TR, Ultrasound shadow of the transverse process of C2. (From Eichenberger U: Anesthesiology, Volume 104[2]. 2006;303-308.)20

SCM SC

LS LC SMC

Cranial

C2-3

C3-4

Caudal C4-5

Medial branch C3 Third occipital nerve Figure 34-4  Ultrasound image longitudinal view (LV) along the articular pillars from C2 to C5. LC, Longissimus capitis muscle; LS, ­Levator scapulae muscle; SC, Splenius capitis muscle; SCM, Sternocleidomastoid muscle; SMC, Semispinalis capitis muscle. (From Eichenberger U: Anesthesiology, 104[2]:2006;303-308.)20

Blockade of the third occipital nerve (formed by the medial or sensory branch of C3) with local anesthetic alone or with corticosteroid as it crosses the C2-3 zygapophysial joint can also be diagnostic and therapeutic for occipital neuralgia, especially where blockade of the greater/lesser occipital nerve does not provide sustained relief, or where there is both spondylitic neck pain and symptoms of occipital neuralgia.20 Both fluoroscopically and ultrasound-guided techniques have been described for this (Figs. 34-4 to 34-6).20,21 If blockade of this nerve(s) provides only temporary relief, radiofrequency lesioning (RFL) can be performed of the third occipital nerve and C3 medial branch to provide long-lasting relief of occipital neuralgia.22,23

Potential Treatment Complications The anesthetic block of the greater or lesser occipital nerve is considered relatively safe. Contraindications to this block include coagulopathy or current infection. Potential complications include bleeding, infection, nerve injury, seizure from intravascular injection of local anesthetic, and headache exacerbation. Care must be given not to puncture the posterior occipital artery. If the artery is punctured, then pressure should be applied vigorously. Surgery with dorsal rhizotomy of C1-4, has been described with about 71% to 77% of patients reporting significant benefit.6,24-26 Before dorsal rhizotomy, local anesthetic blockade of the suspected

34

308  Peripheral Nerve Blocks

A

Figure 34-5  A lateral radiograph of the upper cervical spine showing a needle in place to block the third occipital nerve, the course of which is   shown by the dotted lines. (From International Spinal Injection Society ­Practice Guidelines for Lateral Atlanto-Axial Joint Blocks; with permission.   From Bogduk N: The neck and headaches. Neurol Clin. 2004;22(1):151-171.)

medial (sensory) branches should be performed for diagnostic purposes. Surgical neurolysis with excision of the greater and/or lesser occipital nerve has been described with 80.5% of patients experiencing 50% or greater pain relief.27 Botulinum toxin A injection into the greater occipital nerve has also been described.3,28

B Figure 34-6  Occipital nerve stimulation. Radiograph (A) and schematics (B) of the midline subcutaneous approach in surgical lead positioning for electrical stimulation of the occipital nerve. A, Bilateral position of subcutaneous Resume leads (arrows) after initial adjustment and just before intraoperative stimulation testing. Note that both leads are at the level of C1-2 dens and aimed laterally. B, Schematic of the lead positioning in the subcutaneous occipital area. Note that the lead cable extensions form the loop just below   the implant’s position and via the same midline incision. (From Kapural L,   Mekhail N, Hayek SM, et al: Occipital nerve electrical stimulation via the midline approach and subcutaneous surgical leads for treatment of severe occipital neuralgia: A pilot study. Anesth Analg. 101:171-174, 2005.)

Occipital Neuralgia  309

REFERENCES   1. Loeser JD, ed. Bonica’s Management of Pain. 3rd ed. Philadelphia: ­Lippincott Williams & Wilkins; 2001.   2. Natsis K, Baraliakos X, Appell HJ, et al. The course of the greater occipital nerve in the suboccipital region: A proposal for setting landmarks for local anesthesia in patients with occipital neuralgia. Clin Anat. 2006;19:332-336.   3. Volcy M, Tepper SJ, Rapoport AM, et al. Botulinum toxin A for the treatment of greater occipital neuralgia and trigeminal neuralgia: A case report with pathophysiological considerations. Cephalalgia. 2006;26: 336-340.   4. Slavin KV, Nersesyan H, Wess C. Peripheral neurostimulation for treatment of intractable occipital neuralgia. Neurosurgery. 2006;58: 112-119.   5. Kapural L, Mekhail N, Hayek SM, et al. Occipital nerve electrical stimulation via the midline approach and subcutaneous surgical leads for treatment of severe occipital neuralgia: A pilot study. Anesth Analg. 2005;101:171-174.   6. Kapoor V, Rothfus WE, Grahovac SZ, et al. Refractory occipital neuralgia: Preoperative assessment with CT-guided nerve block prior to dorsal cervical rhizotomy. AJNR Am J Neuroradiol. 2003;24:2105-2110.   7. Rizzo TD. Occipital neuralgia. In: Frontera WR, Silver JK, eds. Essentials of Physical Medicine and Rehabilitation. Philadelphia: Hanley & Belfus; 2001.   8. Hammond SR, Danta G. Occipital neuralgia. Clin Exp Neurol. 1978;15: 258-270.   9. Star MJ, Curd JG, Thorne RP. Atlantoaxial lateral mass osteoarthritis. A frequently overlooked cause of severe occipitocervical pain. Spine. 1992; 17(Suppl 6):S71-S76. 10. Kuhn WF, Kuhn SC, Gilberstadt H. Occipital neuralgias: Clinical recognition of a complicated headache. A case series and literature review. J Orofac Pain. 1997;11:158-165. 11. Hecht JS. Occipital nerve blocks in postconcussive headaches: A retrospective review and report of ten patients. J Head Trauma Rehabil. 2004;19:58-71. 12. Mason JO III, Katz B, Greene HH. Severe ocular pain secondary to ­occipital neuralgia following vitrectomy surgery. Retina. 2004;24:458-459. 13. Knox DL, Mustonen E. Greater occipital neuralgia: An ocular pain syndrome with multiple etiologies. Trans Sect Ophthalmol Am Acad Ophthalmol Otolaryngol. 1975;79:OP513-9. 14. Fredriksen TA, Hovdal H, Sjaastad O. “Cervicogenic headache”: clinical manifestation. Cephalalgia. 1987;7:147-160.

15. Franzini A, Leone M, Messina G, et al. Neuromodulation in treatment of refractory headaches. Neurol Sci. 2008;1:S65-S68. 16. Amin S, Buvanendran A, Park KS, et al. Peripheral nerve stimulator for the treatment of supraorbital neuralgia: A retrospective case series. Cephalalgia. 2008;28:355-359. 17. Gille O, Lavignolle B, Vital JM. Surgical treatment of greater occipital neuralgia by neurolysis of the greater occipital nerve and sectioning of the inferior oblique muscle. Spine. 2004;29:828-832. 18. Rasskazoff S, Kaufmann AM. Ventrolateral partial dorsal root entry zone rhizotomy for occipital neuralgia. Pain Res Manag. 2005;10:43-45. 19. Stojanovic MP. Stimulation methods for neuropathic pain control. Curr Pain Headache Rep. 2001;5:130-137. 20. Eichenberger U, Greher M, Kapral S, et al. Sonographic visualization and ultrasound-guided block of the third occipital nerve: Prospective for a new method to diagnose C2-C3 zygapophysial joint pain. Anesthesiology.­2006;104:303-308. 21. Bogduk N. The neck and headaches. Neurol Clin. 2004;22:151-171. 22. Lord SM, Barnsley L, Wallis BJ, et al. Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl J Med. 1996;335:1721-1726. 23. McDonald GJ, Lord SM, Bogduk N. Long-term follow-up of patients treated with cervical radiofrequency neurotomy for chronic neck pain. Neurosurgery. 1999;45:61-67. 24. Koch D, Wakhloo AK. CT-guided chemical rhizotomy of the C1 root for occipital neuralgia. Neuroradiology. 1992;34:451-452. 25. Ehni G, Benner B. Occipital neuralgia and the C1-2 arthrosis syndrome. J Neurosurg. 1984;61:961-965. 26. Dubuisson D. Treatment of occipital neuralgia by partial posterior rhizotomy at C1-3. J Neurosurg. 1995;82:581-586. 27. Ducic I, Hartmann EC, Larson EE. Indications and outcomes for surgical treatment of patients with chronic migraine headaches caused by occipital neuralgia. Plast Reconstr Surg. 2009;123:1453-1461. 28. Martelletti P, van Suijlekom H. Cervicogenic headache: Practical app­ roaches to therapy. CNS Drugs. 2004;18:793-805. 29. Waldman SD. Greater and lesser occipital nerve block. In: Waldman SD, ed. Atlas of Interventional Pain Management. 2nd ed. Philadelphia: Saunders; 2004:23-26. 30. Kapural L, Stillman M, Kapural M, et al. Botulinum toxin occipital nerve block for the treatment of severe occipital neuralgia: A case series. Pain Pract. 2007;7:337-740.

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Epidural Steroid Injections: Cervical, Thoracic, and Lumbar: Transforaminal, Interlaminar, and Caudal

35

Milton H. Landers, DO, PhD, and Charles N. Aprill, MD A little learning is a dangerous thing; Drink deep or taste not from the Pierian spring: There shallow draughts intoxicate the brain, And drinking largely sobers us again. Alexander Pope

History The term epidural merely denotes a space within the spinal canal but is applied to a variety of injection procedures. They may be classified as to region of interest: cervical, thoracic, or lumbar, and route of administration—caudal, interlaminar, or transforaminal. Each procedure involves directing a needle to a specific target employing an imaging modality to guide and document final needle position. This chapter limits discussion to fluoroscopic guidance. All of these procedures require injection of a contrast material to demonstrate the dispersal pattern of the injectates and documentation of that pattern with spot films. Finally, a report detailing the procedure, including specific technique, details of injected solutions (contrast material, local anesthetic, and corticosteroids), and recording the initial outcome is prepared for the permanent record. There is a report in English literature that refers to the ­caudal injection approach for pain management in 1930.1 The first recorded use of corticosteroids injected into the epidural space for the treatment of “sciatica” was in 1952.2 The route of administration was one of the dorsal foramina of the sacrum, an early, blind, transforaminal technique. This technique was employed in Europe in the 1950s and 60s.3 Interlaminar approaches to the lumbar epidural space were reported in the 1960s.4-6 Caudal and interlaminar techniques became standard practice in the United States, Britain, and most of continental Europe for the next quarter century. Interest in the transforaminal approach reemerged in the last quarter of the 20th century, in an attempt to deliver more target-specific injections.7-9 The cervical literature is sparse by comparison to that of the lumbar spine. The interlaminar approach for epidural injections was generally used in the 1980s.10-12 Cervical transforaminal injection was first reported in 1988.13 A descriptive outcome study by Bush and Hillier employing this approach followed in 1996.14 The transforaminal approach was adopted to deliver therapeutic agents to more specific targets influenced by observations that lumbar

transforaminal injections appeared to be effective in treating lumbar radicular pain.15,16 There are few reports of the origin of thoracic epidural steroid injections (ESIs) for treatment of spinal pain.17,18 A specific technique for thoracic transforaminal epidural injection was described in 2001.19 A recent systematic review revealed an increase in the number of lumbosacral spine injection procedures performed in the last decade of the twentieth century. There was an increase of more than 270% noted between 1994 and 2001.20 Forty percent of these procedures were associated with the diagnosis codes for “sciatica,” “radiculopathy” or “herniated disc.” “Axial low back pain” diagnoses accounted for 36% and “spinal stenosis” 23%. A study of the Medicare population between 1993 and 1999 revealed that the annual number of cervical, thoracic, and lumbar epidural steroid injections peaked at more than 680,000 in 1998.21 These studies focused on the Medicare population, but it is likely that similar increases would be found for the general adult pain population. A review of conservative care for sciatica published in 2000 surveyed 19 randomized controlled trials and pooled odds ratios calculated for several treatment types. The data indicated, “Epidural steroids may be beneficial for subgroups of nerve root compression.”22 In 2009, Lavin published results of an extensive MEDLINE/ PubMed search and searches of large review articles on the major interventional spine topics. This review was performed to find all prospective, double-blind, randomized, placebo-controlled trials in the English language interventional spine literature. He concluded “Fluoroscopically guided lumbosacral transforaminal epidural corticosteroid injections are effective in the treatment of acute/subacute lumbosacral radicular pain, and in preventing future surgeries. No firm conclusions were drawn about cervical epidural (CESI) injections or lumbosacral epidural (LESI) injections for the treatment of  chronic radicular pain.23 A study of the American Society of Anesthesiologists (ASA) Closed Claims Project database revealed that epidural steroid injections account for more complications than any other interventional pain procedure.24 313

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Relevant Anatomy The spinal epidural space is a continuous potential space in the vertebral canal extending from the foramen magnum to the sacral hiatus, lying between the dural sac and the osseoligamentous wall of the vertebral canal. The epidural space is bounded posteriorly by the lamina and ligamentum flavum. The anterior boundary is formed by the posterior disc margin, the posterior longitudinal ligament and the peridural membrane. This membrane attached to the upper and lower ring apophysis of each vertebra, blends with the disc annulus. It spans the waist of the vertebral body.25 Together these tissues form the floor of the vertebral canal. The lateral boundary of the epidural space is fenestrated by paired root canals or foramina at each segment. The vertebral pedicles lie between the root canals. The dural sac nearly fills the vertebral canal and extends from the foramen magnum terminating in the sacral canal at the level of the S1 to S2 segments. There is some variability and the thecal sac may terminate as high as the lumbosacral interspace or may extend to S3. At each vertebral segment paired dural root sleeves extend toward the root canals. The cervical and thoracic dural root sleeves are short and nearly horizontal in orientation, traversing the center of their respective root canals. The lumbar root sleeves are longer, increasing slightly in length and downward angle from L1 to the sacrum. Lumbar root sleeves turn laterally into grooves in the vertebral bodies and pedicles and are in intimate proximity to the medial/inferior border of the pedicles. This is the entrance zone of the root canal, or lateral recess of the vertebral canal. The dural root sleeve contains the dorsal and ventral rootlets of the segmental nerve. The dorsal ganglia lie generally in the midzone of the root canals, between the pedicles of adjacent vertebra. The dura and arachnoid membranes form a “watertight” seal at the proximal end of the ganglia. Cerebrospinal fluid (CSF) fills the root sleeve but does not extend beyond the ganglia. Occasionally ectasia of a dural root sleeve will occur, resulting in extension of the subarachnoid space beyond usual boundaries. Referred to as cystic root sleeve dilatation or Tarlov cysts, they usually communicate freely with the subarachnoid space.26 They may occur at any level of the spine but are most frequent in the sacral region. Usually asymptomatic, they are rarely associated with symptoms.27 There are accumulations of fat in the posterior vertebral canal, deep to the ligamentum flavum and posterior to the dural sac in the thoracic and lumbar spine.28 This posterior fat pad may be small or absent at the L5-S1 level when the dural sac is full size and is applied close to the lamina and ligamentum flavum, as it frequently is. Additional accumulations of fat are found laterally at the level of the discs within the root canals. There is little fat in the cervical epidural space. Midline sagittal spin echo (SE) T1 images of the spine demonstrate the lumbar and thoracic fat pads quite well. Fat is rarely visualized in the vertebral canal above the C7-T1 level. Ample fat fills the vertebral canal below the termination of the dural sac in the sacral vertebral canal. A thin anterior membrane extends from the posterior longitudinal ligament to the anterior surface of the dural sac. This ventral meningovertebral ligament forms a nearly continuous septum, that functionally divides the ventral epidural space into left and right compartments in the lumbar region.29 A midline dorsal connective tissue band fixes the dural sac to the flaval ligaments. The appearance of the band varies from strands of connective tissue to a complete membrane.30

A plexus of valveless veins occupies the anterior epidural space.31 Paired anterior internal epidural veins run the length of the vertebral canal. There are numerous interconnecting veins crossing the floor of the canal, the anterior internal vertebral venous plexus (AIVV).32 A smaller posterior internal venous plexus lines the roof of the epidural space in the lumbar and thoracic regions. Extending laterally around the vertebra, the peridural membrane encloses veins that course around the body of the vertebra.25 These veins communicate freely with the basivertebral veins, at the center of the posterior wall of each vertebral body and the anterior internal vertebral venous plexus. Several radicular veins traverse each root canal. They lie predominantly in the ventral root canal and connect the epidural venous plexus with the ascending lumbar veins and the vena cava. Segmental arteries traverse the root canals at all spinal levels.33 They course in the anterior superior root canals along the anterior superior aspect of the segmental dural root sleeve. Some arterial branches perfuse the dorsal ganglia and segmental neural elements and, as such, are radicular arteries. Other branches penetrate the dura running along the segmental rootlets and may anastomose with the anterior spinal artery. They are, therefore, medullary arte­ ries. Varying numbers of medullary arteries of differing sizes are found in the cervical, thoracic, and lumbar region, and contribute to the blood supply of the spinal cord. The radicular and medullary arteries of the cervical spine arise primarily from the vertebral artery.34,35 Some arise from the ascending cervical and posterior cervical arteries. Medullary arteries penetrate the dura and divide into anterior and posterior branches, eventually reaching the anterior and paired posterior spinal arteries. Cervical medullary arteries are variable in size and distribution. There are usually two or three arteries of moderate size in the adult. They may be present at any segment and on either side.36,37 The upper and midthoracic cord is supplied by medullary arteries arising from branches of the costocervical trunk and spinal branches of the aorta. There is usually a single large medullary artery arising from the aorta and supplying blood to the lower half of the thoracic cord and conus. This large medullary artery, the artery of Adamkiewicz, has a variable origin but usually originates on the left side (80% of patients), between T7 to L4, most often between T9 and T11.38 In a study of 4000 spinal cord angiograms, there were three instances in which the major medullary artery of the distal thoracic cord originated at the fourth lumbar artery.39 Paired lumbar arteries originate from the aorta at each lumbar segment. These give rise to spinal branches that include radicular and medullary branches.40 Most lumbar spinal branches are small. Some may be 1.0 to 2.0 mm in diameter. There is potential for a medullary artery of substantial size to be present in any root canal.41

Spondylogenic Pain Spondylogenic pain arises from a component of the spine or its supporting structures, and is synonymous with other terms such as nonspecific or idiopathic spinal pain. The International Association for Study of Pain (IASP) published a taxonomy, defining clinical terms used to describe pain, in an effort to standardize the use of terms.42 Somatic pain results from noxious stimulation of a musculoskeletal component of the body and arises as a result of stimulation of nociceptive nerve endings in bone, ligament, joint, muscle or tendon. Visceral pain occurs with noxious stimulation of a body organ or its capsule. Both somatic and visceral derangements cause

Epidural Steroid Injections: Cervical, Thoracic, and Lumbar: Transforaminal, Interlaminar, and Caudal  315

pain in the location of the source structure, but it is often vague and ill defined. Referred pain is pain perceived in areas adjacent to or remote from the source of pain. Convergence is the physiologic basis for referred pain. Sensory neurons from different peripheral sites converge on common neurons in the spinal cord and thalamus that relay to higher centers in the brain. Without additional sensory input, the brain may not be able to determine the specific site of the initial input. Referred pain is a misperception of the origin of the signal that reaches the brain. Somatic spinal pain syndromes may be expressed topograph­ ically as neck, midback, or low back pain. Local pain in these areas is often accompanied by referred pain. Somatic neck pain may be perceived with pain referred to the shoulder girdle or upper extremity. Lesions of the midback refer to the chest wall and low back pain is commonly associated with pain in the buttocks and lower extremity. Somatic referred pain is typically diffuse, deep, and ill defined, aching in quality and aggravating. Radicular pain occurs when there is irritation or injury of a spinal nerve or its roots. In the lumbar spine, simple compression of a normal nerve or nerve root does not provoke pain.43 Alone, pressure on a spinal nerve or its roots may produce a conduction block of axons. Sensory axon conduction block results in loss of sensation or “numbness.” Motor axon block results in weakness. Compression alone can result in radiculopathy, without radicular pain. Pressure on a previously injured or damaged nerve or root provokes pain. Local ischemia or inflammation can induce ectopic impulses in a dorsal root canal ganglion resulting in radicular pain. Lumbar radicular pain is discretely localized, “bandlike” in distribution, and shooting, lancinating, or shocking in quality44 and can have a cutaneous component.

Preprocedure Evaluation A practitioner of spinal interventions may be a managing physician directing the care of a patient with a painful spinal condition or a consultant to whom a patient has been referred for a procedure. With each encounter, the responsibility for assessing the clinical condition and the appropriateness and risks of a given procedure, rests with the physician injectionist. The practitioner must attempt to understand the pain and associated disability. The patient is the primary source of that information. What is the primary complaint? Is this an acute or chronic problem; a constant or recurring problem? Is local pain somatic or visceral? Is there a radicular or somatic referred component? One must localize the somatic component and the location of radiating pattern. The character and intensity are as important as the location. What are the mechanical aspects, that is, what provokes and relieves the pain? An example: A 35-year-old female presents with recent onset of left posterior and lateral aching neck pain for no apparent reason. Constantly present, the aching varies from moderate to severe on occasion. There is diffuse aching of left poster­ ior shoulder girdle muscles. She has recurring episodes of severe, “sharp, stabbing” left upper extremity pain, extending along the posterior arm, medial forearm, and into the left long finger. No arm weakness, frequent “tingling” of the whole upper extremity and normal strength and reflexes are observed. Prolonged sitting, particularly at a console or working at a desk, aggravates the neck pain. Neck extension and left side bend induces a painful “shocking” sensation in the left arm. Though intermittent, the arm pain is the

dominant complaint. She has axial somatic neck pain, with somatic referred pain to the left shoulder girdle and left upper extremity radicular pain, without radiculopathy. Self-pain rating, employing a specific method such as the visual analog scale (VAS) is essential. What is the intensity rating at the time of assessment? Range of intensity is determined by noting the pain rating at its best and worst. Patients can express their pain on pain drawings, which should be correlated with the description of symptoms. These instruments are very useful in assessing the immediate response to an intervention. Simple psyche screening questionnaires to assess anxiety, depression, self-perception of disability, and somatization are useful in assessing pain behavior. What has been the response to any previous interventions or procedures? Finally, what medications, at what doses have been used to treat and what has been the response? Psychological factors contribute to pain and influence the outcome of interventions. There is no simple screening tool. Therefore, one must know his or her patient and history. Medical history includes review of all allergies and idiosyncratic reactions, any current illness or infection and chronic conditions such as cardiovascular disease, diabetes, seizures, respiratory and renal disorders. All these factors affect how procedures will be performed. The history of all surgical procedures and their outcomes should be explored. A complete list of current medications is mandatory. A general review of systems should include information about sleeping pattern. Social habits such as tobacco and alcohol use or abuse are important. Patient’s work and/or avocations may pertain to complaints and should be explored. A family history may contribute to recognition of an underlying hereditary disorder. The physical examination on a first encounter is general but with focus on primary and secondary complaints. Developmental status, any deformities or postural aberrations should be recorded. The level of distress during interview and examination, patient’s willingness and ability to cooperate with interview/examination and the patient’s demeanor and orientation should be observed and recorded along with routine vital signs. Examination may include assessment of gait and both sitting and standing postures. Passive or active movements of the cervical, thoracic, or lumbar spine through their range of motion are observed. Palpation of regional musculature and bony prominences helps to localize somatic pain. Epidural procedures are injections into the spinal neuraxis and require a basic neurologic examination prior to the procedure. On a case-by-case basis, examination of core and extremity strength, weakness, range of motion, and reflexes contribute to formulating a working hypothesis. Spine imaging plays a definite role in the evaluation of spine pain complaints both in demonstrating relevant pathology and aiding in planning a safe and efficient approach for procedures. Modern imaging modalities provide excellent depictions of spine anatomy. However, many lesions, evident in the maturing spine, are clinically insignificant.45 Imaging studies often demonstrate pathology that is irrelevant. Computed tomography (CT) or magnetic  resonance imaging (MRI) may demonstrate a left C3-4 disc protrusion in a patient complaining of right arm pain and altered sensation radiating to the right forearm, thumb, and index finger. It cannot be overstated that there is a significant incidence of pathology in asymptomatic subjects.46 A focal disc protrusion on the right at L3-4 may be clearly defined by MRI, in a patient complaining of left buttock pain extending to the left calf.47 Scans should be reviewed overall, but with particular attention to areas that might be related to the patient’s underlying complaints, as gleaned from the interview and

35

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examination. One should carefully study the left L4-5 and L5-S1 root canals in a patient with pain extending from the left buttock to the left anterolateral leg and dorsum of the foot. Recently 150 patients with unilateral leg pain, and MRI confirming neural compression by prolapsed disc or foraminal stenosis had lumbar transforaminal epidural injections (LTFE) at appropriate sites. These were effective in relieving their pain initially, and only18% of these patients required surgery at a minimum 1-year follow up.48 Not all abnormalities need be targeted but rather those most likely to be associated with the expressed symptoms and ­physical findings. Indications: This clinical process should provide a basis for a hypothesis as to the nature of the underlying spinal disorder. Epidural injections are indicated when a patient expresses constant or frequently recurring episodes of radicular pain, but also patients with somatic spinal pain associated with mixed somatic referred and radicular pain referred to one or both extremities or the chest wall. Contraindications: Absolute contraindications include a bleeding diathesis, systemic infection or local infection in the procedure field, pregnancy, and inability or unwillingness to cooperate and participate in the procedure. Relative contraindications include significant competing disease—that is, uncontrolled hypertension, diabetes, congestive heart failure, and anticoagulation therapy. There is risk of a major depressive disorder in patients with chronic pain. Pure psychogenic pain is rare and used pejoratively. Almost all chronic pain can be altered by psychological adjustments and issues. Without these being addressed, successful diagnosis and treatment is unlikely. Absolute contraindications include active psychosis and homicidal or suicidal ideation. Studies have shown a relationship between physical and sexual abuse and various types of pain. Correlation of failed low back surgery with childhood trauma has revealed definite risk factors. These include physical, psychological, and/or sexual abuse, emotional neglect, abandonment, and chemical dependence and/or loss of a primary caregiver.49-51 Relative contraindications include personality disorders, bi-polar disorder, severe depression, lack of social support, and drug dependence/abuse. Negative predictors are external locus of control, “just fix me,” unstable relationships, poor vocational adjustment, neurocognitive deficits, inability or unwillingness to participate in active rehabilitation, unreasonable expectation of procedures, ongoing litigation, symptoms inconsistent with pathology, high fear avoidance, inability to actively exercise, and catastrophizing cognitive style. Positive predictors are history of adherence to treatment regimen, positive support system, compliance (currently and historically), and appropriate expectations.

A Few Medical Issues Vasovagal Vasovagal responses are not rare. About 1 in 14 patients undergoing cervical interlaminar epidural injection will experience a vagal response. Incidence varies by gender, women are at greater risk than men and with procedures, vagal response is five times more common in cervical than in lumbar procedures. Although they are usually a minor complication, vasovagal events may be quite severe. Vigilant screening is necessary to discover previous episodes; suspect “fainters.” Pretreat with atropine when suspicious and recognize the early signs (i.e., “I feel sick,” nausea, and slowing of pulse rate).

However, these doses are much in excess of those required for any interventional pain procedure.

Contrast Material Allergic reactions to modern contrast materials are extremely rare. Some may be related to preservatives such as methylparaben. Wang reviewed 84,928 intravenous contrast injections noting “allergic” reactions in 545 (0.6%).52 Seventy seven percent of the reactions were “mild,” primarily urticaria, successfully treated with diphenhydramine. Twenty one percent had moderate reactions with respiratory symptoms, facial edema, or both. Corticosteroids intravenously or by inhaler were effective in controlling these reactions. Two percent, eight women and three men, had severe reactions (0.0012%). Three were unresponsive; frank cardiorespiratory arrest occurred in one. There were no deaths and no long-term sequelae in 10 of the 11 patients with severe reactions. Contrast material is employed to document where the injectate is spreading and to determine where it is not spreading. Modern nonionic contrast agents are safe for all epidural injections. Unintentional vascular or even subarachnoid spread will cause no problem. In those very rare instances of documented history of severe allergic reaction to nonionic contrast material, gadolinium may be employed as a substitute radiography contrast agent.53 Diabetics taking metformin are at risk for contrast material nephropathy (CMN) if exposed to nonionic contrast material, during radiographic procedures. Solomon found no change in renal function in those subjects who had normal renal function prior to testing.54 However, some patients with normal renal function exhibited increases of serum creatinine with high-contrast loads.55 This should not be a problem with epidural injections because the contrast doses employed are limited and much lower than the volumes delivered in the radiologic procedures. Doses in excess of  100 mL are not unusual for enhanced CT or angiograms. However, diabetic patients with renal impairment should discontinue metformin, with approval of their primary physician.

Local Anesthetics The local anesthetics employed in the epidural injections are lidocaine and bupivacaine. These amides are primarily metabolized in the liver and excreted in the urine. Their allergic potential is extremely low. Ester-based local anesthetics (procaine) have a higher incidence of allergic reaction. A large survey attests to the overall safety of the amides as spinal anesthetics.56 For epidural injections, lidocaine may be employed in concentrations of 0.5% to 4.0% and bupivacaine at 0.25% to 0.75%. The percentage concentration of the anesthetic is reduced with increasing volume delivered. Although central nervous system and cardiovascular system toxicity can occur following the epidural, intravenous, or subarachnoid injection of local anesthetics, the toxic doses are far greater than the volumes employed in epidural injections—40 mL of 1.0% lidocaine (400 mg) delivered to the epidural space of test subjects resulted in average peak plasma concentrations safely below neurotoxic levels.57 One author recommended the maximum epidural dose of lidocaine to be 500 mg and 225 mg for bupivacaine.58 Acute cardiac complications, decreased cardiac output being one, can occur from intravascular injection of lidocaine or bupivacaine. Study has shown that normal cardiac function is maintained in subjects with lidocaine plasma levels of 4 to 8 mcg/mL. Plasma levels this high require doses of >400 mg of lidocaine.59 In human

Epidural Steroid Injections: Cervical, Thoracic, and Lumbar: Transforaminal, Interlaminar, and Caudal  317

volunteers slow intravenous (IV) injection of bupivacaine to produce plasma concentrations equivalent to those achieved during epidural injections did not cause significant cardiovascular change.60 Between 3.0 and 7.0 mL of low concentrations of anesthetics for interlaminar injections and 0.75 to 2.0 mL of higher concentrations for transforaminal injections are not toxic in the epidural space. These doses are not toxic if technical misadventure results in delivery to the vascular system or subarachnoid space. Because of the longer half-life of bupivacaine, this anesthetic should be avoided in interlaminar epidural injections, particularly in the cervical spine. Inadvertent delivery into the subarachnoid or subdural space results in prolonged effects, specifically affecting respiratory function with misplaced cervical injection. Decreased concentration of anesthetics must be considered for interlaminar epidural injections in the cervical and thoracic regions in patients with respiratory or cardiovascular health problems because decreased cardiac output and heart rate can occur with sympathetic blockade, which occurs to some degree with all interlaminar epidural injections.

Corticosteroids The steroid preparations most frequently employed in ESI are methylprednisolone acetate, triamcinolone acetonide, betamethasone sodium phosphate, betamethasone acetate, and dexamethasone sodium phosphate. All corticosteroids have systemic effects when injected in the epidural space. Side effects may include: fever, myalgia, malaise, fluid and electrolyte imbalance, hypertension, hyperglycemia, myopathy, ulcers, immunosuppression, behavioral changes, allergic reaction, and pituitary-adrenal suppression. Abrupt withdrawal after prolonged oral use may precipitate acute adrenal insufficiency. Most of these side effects are clearly associated with the systemic absorption of corticosteroid and subsequent transient hypercorticism, and likely account for many of the “minor” complications associated with epidural injections. The cardiovascular system is affected directly and indirectly. Direct effects are due to steroid receptors on heart and smooth muscle. Indirectly, steroids increase sodium uptake and vascular tone, raising blood pressure. Judicious use is prudent in patients with cardiac disease, hypertension, and congestive failure. Dose and frequency of administration must be carefully monitored in this group. In the central nervous system, nerve tissues exhibit increased excitability, EEG abnormalities are seen, subjects experience euphoria and behavioral changes. Rarely, these effects can be severe. A  case report describes 67-year-old male who developed psychotic episodes within a week of a cervical ESI, along with other steroid injections in one treatment session. The symptoms spontaneously resolved in approximately 7 to 10 days.61 This case serves to remind us that we must always be cognizant of the doses we deliver, and remember patients may be receiving “steroid shots” from other physicians for unrelated problems. Endocrine system alterations include decreased adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), and follicle-stimulating hormore (FSH), and testosterone. The changes are largely dose related. Bizarre responses do occur rarely. A 24-year-old man underwent a second cervical ESI of 60 mg of methylprednisolone for ongoing severe arm pain. A cushingoid appearance developed 1 month later. Serum cortisol was undetectable, there was no adrenal response to synthetic ACTH, and urinary-free cortisol was below normal at 12 weeks. Cortisol normalized in 4 months, however, the patient’s cushingoid appearance persisted for 12 months.62

An epidural steroid injection of 160 mg of methylprednisolone will suppress adrenal function for weeks.63 Does injection of corticosteroids increase the risk of infection? Infections do occur in patients following ESIs.64 Postoperative infections are increased in hip replacement patients who received preoperative steroid injections.65 No studies have been done on outcomes of spine surgery after ESI, but suppression of the immune system suggests there is inherent risk, especially in the first 4 weeks post injection. Epidural administration of glucocorticoids results in potent suppression of insulin action. This should be taken into account when patients with diabetes receive ESIs.66 Lumbosacral transforaminal and caudal epidural betamethasone injections are associated with statistically significant elevations in blood glucose levels in diabetic subjects. This effect peaks on the day of the injection and lasts approximately 2 days.67 The administration of three epidural injections (250 mg prednisone equivalent) was followed by suppression of the corticotropic axis that persisted beyond 21 days. Plasma cortisol and ACTH and urinary free cortisol were markedly reduced at the day 1 and day 7 posttreatment visits, compared to baseline. At 21 days, these variables were still diminished.68 We must be vigilant in follow-up of our diabetic patients. The musculoskeletal system suffers from some bone mineral density loss, muscle weakness and wasting, and predisposition toward avascular necrosis with long-term oral steroid use. Although systemic corticosteroids may be associated with loss of bone mineral density, a prospective study of 204 patients followed for 1 year after standard doses of epidural steroids revealed no change in bone mineral density.69 The currently used steroids contain preservatives. Bernat thought that seizures following intrathecal cortisone acetate were due to the preservative, 0.9% benzyl alcohol. Benzyl alcohol is common in depot steroids and is neurotoxic.70 Hodgson reported that there was no concrete evidence of neurotoxicity of intrathecal steroids, but did not recommend purposeful delivery of these agents into the subarachnoid space.56

Major Complications Directing a needle deep into the tissues in and about the spine approaches sensitive spaces and structures of the neural axis. There is a spectrum of possible major complications.

Infection Infection following epidural injection is a serious issue. It has been described as a rare complication.71 However, the possibility of procedure-related infection must be a concern for the injectionist. Analysis of the American Society of Anesthesiologists (ASA) Closed Claims database from 1970 to 1999 revealed that infection was the third most common complication of chronic pain procedures, accounting for 13% of all complications.24 Any penetration of the skin surface with a needle then placed in deep spaces in and about the spine has the potential of introducing organisms with subsequent infection.72 Standard aseptic preparation and draping of the local injection site and good aseptic technique will minimize this complication. Diabetic and immunocompromised patients are a subgroup that should be recognized prior to procedures. Antibiotic prophylaxis should be considered for immunocompromised patients undergoing ESI.73 Antibiotics should not be mixed with the contrast during any epidural injection.

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Accidental delivery of antibiotics into the subarachnoid space must be avoided.

Bleeding/Hematoma Many veins lie in the needle path or near endpoint targets of transforaminal epidural injections (TFESI). Furman and colleagues reported the incidence of fluoroscopically confirmed “vascular uptake” occurring during lumbar74 and cervical75 transforaminal injections. Observing blood at the needle hub reliably predicts intravascular injection, (97% specific). But this finding has low sensitivity, (45% overall). The absence of blood in the needle hub despite aspiration is not reliable. The incidence of vascular uptake with lumbar procedures is about 11%. There is a higher incidence in the cervical spine where confirmed intravascular injection was observed in nearly 20% of patients. Kim and coworkers have recently reported a much higher rate of vascular uptake for cervical transforaminal injections, more than 50%.76 Although neither author specified, most of the vascular uptake seemed to be venous. No complications occurred. Venous uptake during epidural injections is common and innocuous as long as it is recognized and needle adjustment is made before injecting physiologic solutions. Veins are less abundant in the posterior epidural space and venous uptake is less frequently seen during interlaminar epidural injections. Three surveys of cervical interlaminar epidural injection on more than 2200 patients claim no major complications.76-78 Minor adverse responses, such as increased headache, insomnia, vasovagal episodes, facial flushing, dural puncture, and short-term nocturnal fever were encountered. Similar response profiles occur with thoracic79 and lumbar interlaminar injections and caudal epidurals as well. Most of these are likely a response to the corticosteroid and are unavoidable for the most part. The incidence of epidural hematoma is approximated to be less than 1 in 150,000 epidural injections.80 Clinically relevant hematoma may occur at any level, the majority of reported cases were associated with injections in the cervicothoracic area. Spinal epidural hematoma causing acute myelopathy is a rare complication. In a case report, Stoll and colleagues noted epidural hematoma after ESI in a young man with no predisposing factors.81 An older patient with apparently normal coagulation received multiple cervical ESIs for palliative pain control over several years. A hematoma that required surgical decompression occurred following the seventh procedure.82 The potential for bleeding and hematoma formation is increased in patients with a coagulopathy, liver disease, or in patients taking anticoagulant medications. It is crucial that the injectionist be familiar with a patient’s coagulation status and with common anticoagulant and antiplatelet medications.83 Anticoagulant therapy should not be interrupted until there is full understanding of the reason for the therapy. Actual discontinuation of anticoagulant therapy is usually best left to the physician managing and prescribing the patient’s anticoagulation. Epidural injections are elective procedures. Interrupting anticoagulant therapy may increase the risk of serious complications such as stroke, myocardial infarct, or pulmonary embolus. The following guidelines for performing spinal procedures in anticoagulated patients are based on the second American Society of Regional Anesthesia and Pain Medicine (ASRA) Consensus Conference on Neuraxial Anesthesia and Anticoagulation in 2003.80 Warfarin therapy should be discontinued 4 to 5 days before spinal

procedures and the international normalized ratio (INR) should be within normal range at the time of the procedure. Thienopyridine derivatives, (e.g., clopidogrel, ticlopidine) should be suspended 7 days and 14 days, respectively, prior to spinal procedures to allow for recovery of primary and secondary platelet aggregation and platelet-fibrinogen binding. Low-molecular weight heparin should be held for at least 12 hours before the procedure in thromboprophylactic dosing and at least 24 hours in therapeutic dosing. Aspirin and nonsteroidal antiinflammatory drugs have not been found to have any contraindications for spinal procedures. It may be prudent to discontinue full dose aspirin therapy for 10 days in patients undergoing interlaminar procedures.

Dural Puncture During interlaminar epidural injections, the dural sac is at risk. Transforaminal injections place the dural root sleeves at risk. Nonfluoroscopically guided interlaminar injections have increased incidence of dural puncture with prevalence up to 5.0% in cervical epidural injections.84 Dural puncture is reportedly rare when the procedure is performed by “expert” interventionalists.85 Minor complications, including headache secondary to dural puncture occurred in less than 0.5% in more than 4300 procedures. Dural puncture may occur with more frequency in the cervical spine above C7 and at L5-S1. In both areas there may be a paucity of epidural fat with the dural sac juxtaposed against the flaval ligament. Failure to recognize subarachnoid spread results in injection of anesthetic and steroid into the subarachnoid or subdural space. Delivery of anesthetics in sufficient quantity and concentration may produce significant spinal block, most serious at cervical levels where the block may impair respiration. These misadventures are avoided by selection of appropriate target, proper needle, good visualization, a cooperative, comfortable—but minimally sedated—patient and precise technique. Subdural injections between the dural and arachnoid layers are rare but can and do occur. The injectionist must be able to recognize contrast injection into this space as noted by a cystlike appearance. Contrast injected into the subdural space can often be completely aspirated, which is not possible with subarachnoid or epidural injection.

Spinal Cord Puncture Minimal direct cord injury occurs if there is puncture of the spinal cord. Injection of any solution into the substance of the cord is a major problem. Injury is proportionate to the volume of injectate. Direct puncture of the cord provokes pain and altered sensation in most subjects. Injection of solution into the substance of the cord adds to the trauma with ischemic pressure injury at the site of the injection in the cord. Hodges reported two cases of cervical cord injury secondary to cord injection. Both patients were heavily sedated an unable to respond.86 Severe thoracic cord injury occurred when a low thoracic epidural injection was performed under general anesthesia.87 Some cord punctures may not provoke pain.88 Mayall reported permanent paraplegia resulting from multiple attempts at thoracic epidural injection in an awake patient. No lateral view was used during the procedure.89 Surgery subsequently revealed multiple punctures of the cord. These complications are technical misadventures. They are minimized by careful attention and precise technique.

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Brain and Spinal Cord Infarct Arterial filling during transforaminal injections has been rarely reported. Only two cases of cervical medullary artery filling during transforaminal injection have been reported.90,91 In both instances medullary artery filling was recognized during real time fluoroscopy and confirmed, in one instance, with digital subtraction angiography (DSA). Both procedures were aborted without further incident. A single case of lumbar radicular/medullary artery filling during transforaminal injection has been published.92 Filling of a small artery in the central canal during a right S1 transforaminal injection was recognized during real time fluoroscopy, but demonstrated more dramatically with DSA. Transforaminal injections are hazardous because of important arterial structures in the target field. Delivery of a particulate steroid into an artery may result in embolization of particles, larger than capillaries, with subsequent ischemia and/or infarct of the perfused tissue. There were nonpublished, anecdotal reports of catastrophic neurologic complications associated with epidural injections circulating during the last decade. Brouwers and colleagues reported the first such occurrence in 2001.93 The central cervical spinal cord infarct occurred in conjunction with a fluoroscopically guided C6 transforaminal injection. This was likely the result of embolization of the anterior spinal artery watershed by way of a reinforcing cervical medullary artery.37 The next year Houten and colleagues reported the first cases of lower thoracic and conus infarct occurring as a result of lumbar transforaminal injections.94 Two injections were performed at the L3-4 level, one on the left, the other on the right. The third was an injection at S1. The authors implied probable injection into an aberrant artery of Adamkiewicz. A more likely hypothesis is injection into lumbar or sacral radiculomedullary arteries. In 1971, Lazorthes reported observing a well-developed anastomotic circulation to the conus and distal thoracic cord by way of lumbar and sacral arteries. In an experimental study, colloid material was injected into the aortic circulation, below the origin of the artery of Adamkiewicz and was subsequently identified in the distal cord and conus of the experimental animals.41 He postulated that these colloid emboli reached the anterior spinal artery circulation by way of reinforcing lumbar and sacral radiculomedullary arteries. Glaser reported paraplegia following a thoracolumbar transforaminal injection in 2005.95 Yin and Bogduk reported retrograde flow in a radicular arterial branch and subsequent filling of the thoracic anterior spinal artery. Retrograde flow into medullary arteries or the vertebral artery without direct cannulation can occur, providing an alternative mechanism of potential injury to the spinal cord or brain during transforaminal injections.96 Since the first report in 2001, there has been a frightening number of case reports of catastrophic neurologic complications in the literature.97 In a mail-in survey, Scanlon collected 287 responses from physician members of American Pain Society. There were 78 major neurologic complications associated with cervical TFE. All procedures involved injection of particulate steroid preparations. There were vertebrobasilar brain infarcts and cervical spinal cord infarcts. The survey did not explore thoracic spinal cord and conus infarcts. There are more events than case reports; many are encountered in the context of medicolegal proceedings.92 One of the authors (CA) has reviewed six distal thoracic/conus infarcts in the last 2 years, none of which has been reported in the literature.

Kennedy and colleagues reported two cases of distal thoracic cord and conus infarcts that occurred in conjunction with L3 TFE injections. A left L3 TFE was performed with fluoroscopic guidance, using betamethasone (Celestone) as injectate. A right L3 TFE was performed with CT guidance, using methylprednisolone acetate (Depo-Medrol). Paraplegia occurred almost immediately in both cases. Follow-up MRI scans demonstrated typical distal thoracic spinal cord and conus infarcts, with increased signal intensity in the central cord from about T9 to the tip of the conus.98 Prevention of these complications begins with awareness that this can happen. First, recognize intraarterial injection when it occurs.91 Careful real time fluoroscopy, in the frontal plane, during slow injection of an adequate volume of contrast to opacify vessels is mandated. Visualization of vessels can be enhanced by DSA. Second, injection of a small test dose of concentrated local anesthetic before injecting steroids, especially with particulate varieties, to test for onset of neurologic signs may allow recognition of unexpected flow in the vertebral or medullary arteries.99 Currently the presumed mechanism of spinal cord injury is an embolic shower of particles of the steroid preparation into the circulation of the anterior spinal artery.100,101 A third safety measure is to avoid particulate steroids entirely for all transforaminal epidural injections. Dexamethasone sodium phosphate is a nonparticulate steroid. Derby and associates found the particle size in this preparation to be approximately 10 times smaller than red blood cells and they do not appear to aggregate. They have lower density than the particles and aggregates of methylprednisolone acetate, triamcinolone acetonide, and betamethasone sodium phosphate/acetate, the most commonly used agents.100 In a comparison study, Dreyfuss and colleagues reported that dexamethasone was slightly less effective than triamcinolone, but the difference was not statistically significant.102 There have been no reported infarcts when dexamethasone has been used for transforaminal injections. Two animal studies have demonstrated severe neurologic injury to the animals when particulate steroid preparations were injected into the carotid103 and vertebral104 arteries. There was no evident injury to the animals receiving intraarterial injections of the nonparticulate preparation, dexamethasone. A theoretically safer nonparticulate agent appears to be a valid alternative to the particulate agents that have been used to date.

Epidural Injection Techniques Equipment Fluoroscopy Fluoroscopy is mandated for all interventional spinal procedures, including injections performed for the diagnosis or treatment of pain of spinal origin. Although “blind,” nonfluoroscopically guided, interlaminar injections for peri- and postoperative analgesia are the norm in the anesthesia arena, the specialty of interventional pain or non-surgical spine, demands precise needle placement, selective administration of medications, validation of the procedure, and a historical record. The literature105-107documents that in experienced hands, successful epidural needle placement is to be expected in only 60% to 70% of cases where fluoroscopy is not used. A 30% to 40% failure rate does not provide a sufficient probability of success on which to base a diagnostic or therapeutic modality. Therefore, interventional spinal pain procedures performed using

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nonfluoroscopically guided (i.e., blind) techniques should be considered as highly inappropriate and possibly sham, and fraudulent procedures whether being performed for diagnostic or therapeutic objectives. Rationalizations that the cost of fluoroscopy is prohibitive, equipment unavailable, historical precedent, or the “vast experience and skill” of the practitioner, usually belies economic impairment or poor, insufficient training and cannot be used as an excuse for the substandard practice of medicine. It is imperative that all physicians performing fluoroscopically guided spinal injections have training in the interpretation of real time fluoroscopic images whether cervical, thoracic, lumbar, or sacral. This training must be beyond the level of a residency and most current “pain” fellowships. Expertise in radiologic interpretation is far beyond the training and proficiency of nurse anesthetists (CRNAs), physician assistants (PAs), and other so-called “mid level nonphysician providers.” Performance of interventional pain procedures constitutes the practice of medicine as noted by at least one judicial body within the United States,108 and numerous medical specialty societies including the American Medical Association,109 the International Spine Intervention Society,110 and the American Society of Anesthesiologists.111 The fluoroscopic instrument of choice is the C-arm, which can be moved in any plane to provide optimum imaging to direct needle insertion and to verify, and document, final needle position and contrast spread. Radiation-saving modalities such as low dose, pulsed mode, collimation, and saving of last image are essential and ensure safe practice. Digital subtraction imaging (DSI), although not at present standard of care, can provide significant useful information when used correctly. The majority of interventional pain procedures are performed where the C-arm fluoroscope is used to align the skin entry point with the target. A needle can then be advanced parallel to the beam. Using this down-the-beam technique, the correct angle of needle insertion is unmistakable, and when the injectionist is familiar with the anatomy lying between the skin and target, it offers the safest approach. For precise work, parallax demands that the target is placed in the center of the image. To use the C-arm, an x-ray-compatible procedure table is required. Although some operating room tables will suffice, most have metal incorporated into their structure, which limits certain fluoroscopic projections. Carbon fiber tables, with the pedestal at the foot, are now quite affordable and provide unlimited access and unrestricted imaging possibilities. Radiation safety precautions, including the use of lead aprons, thyroid shields, and radiation exposure monitors must be provided for all personnel in the procedure room. Some have advocated the use of lead glasses. One often overlooked aspect of radiation safety is the radiologic technician, RT, actually controlling the C-arm. A competent RT will not only assist in obtaining the correct images for safe needle placement, but should also control collimation and the power output of the fluoroscopy equipment to ensure that the physician performing the procedure is acquiring the least radiation while maintaining adequate imaging quality throughout the procedure. However, obtaining the correct image required for an injection procedure is the responsibility of the physician alone, and the essential “fine tuning” to provide this image is best handled personally. Regarding radiographic guidance, although the use of CT guidance has been advocated by a small minority of radiologists,112 most radiologists within the interventional pain community reject the use of this imaging modality for the placement and validation

of safe needle position. Using CT allows one to accurately delineate the skin entry point; however, the advancement of the needle toward the target is accomplished crudely, without imaging assistance. This adds to the physical discomfort of the patient, the time required to complete the procedure, and the chance for needle misadventures. CT necessitates the injection of contrast for verification of needle placement without the benefit of active, real time imaging. Vascular injections will, in all likelihood, escape detection owing to the rapid “washout” of contrast secondary to blood flow within the vein or artery. In addition, the marked increase in total radiation exposure to the patient, as inherent in CT, should be of concern. No literature exists in which evidence indicates any benefit to the use of CT for routine spinal injections. Specialty group guidelines published by the International Spine Intervention Society (ISIS)113 and the Physiatric Association of Spine, Sports, and Occupational Rehabilitation (PASSOR),114 specifically do not mention CT use for epidural injections, whether transforaminal or interlaminar. As noted previously, severe permanent neurologic sequelae following the use of CT for cervical and lumbar transforaminal epidural injections have been reported in the literature and medical legal documents. These cases involved paraplegia, quadriplegia, and death secondary to cord infarct. A historical record of all procedures must be archived either with hard or digital images. Multiple images must clearly identify that the needle is in safe position prior to injection of contrast, and that the contrast pattern represents a safe flow of the injectate. Miscellaneous Supplies Aseptic technique demands the use of sterile gloves. Although their effectiveness in the control of infection in regard to minimally invasive spinal injections has never been demonstrated, some have advocated the use of masks, hats, and gowns. A sterile cover for the C-arm image intensifier allows the physician to control and direct the image during the periprocedural period. In addition, this prevents contaminating detritus from falling onto the sterile field from the equipment. A sterile, long, 6- to 12-inch, radio-opaque pointer, combined with a skin marking pen enables the injectionist to mark the proposed skin entry site in a radiation safe manner. A variety of needles and syringes are required and these vary according to the specific procedure intended. For interlaminar injections, prepared trays offered by a number of companies are often the most efficient, and cost effective, option. Hustead, Crawford, or Tuohy epidural needles of 18 or 20 gauge, 3.5-inch are ideal for most situations. Occasionally a 5-inch needle is required. Interlaminar injections require the use of tactile sense by tissue resistance for realization of needle tip position during needle insertion. This ability to identify needle tip position by feel is lost when smaller gauge needles, 22 or 25 gauge, are used and will result in a higher incidence of dural puncture. In addition, the valuable identification with aspiration of CSF with intrathecal placement, or blood when intravascular, cannot be relied on if these needlessly small needles are used. The adequate use of local anesthetic renders the insertion of an 18 gauge needle no less comfortable than the use of a smaller gauge instrument. Sharp, cutting needles designed for intrathecal placement, Chiba or Quincke type, were not designed for use in accessing the epidural space via the interlaminar approach because the variation of resistance of the tissue layers trespassed cannot be as readily appreciated. A 5 mL loss of resistance (LOR), glass or plastic syringe is unique to the interlaminar approach. Injections into the most caudal aspect of the epidural space through the

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sacral hiatus can, in most instances, be undertaken with a 25-gauge  1.5-inch needle. Transforaminal epidural injections are best accomplished with 25-or 22-gauge needles. In nearly all cases, 3.5- or 5-inch lengths suffice. Quincke or Chiba beveled needles are used by the majority of experienced practitioners. A small bend of the tip, opposite the bevel, is used by experienced physicians to allow precise directional control during insertion. Occasionally, an intertransverse fusion mass may prevent the direct insertion to the target. This might require the use of a two needle technique: an introducer needle of larger diameter, (18 gauge) placed at the correct target depth, and a procedure needle with a large bend capable of maximum lateral movement, inserted through the introducer. Although some practitioners have advocated the use of blunt needles to prevent unintentional arterial uptake, no evidence exists as to this claim as has been addressed in detail.115 In addition, blunt needles require an introducer needle to puncture the skin, are difficult to control, and (in at least one small study) have been shown not to decrease the incidence of vascular puncture.116 In addition to the procedure needles specific to any technique, a 25-gauge needle for skin localization and an 18 gauge for drawing up of medications are used. Syringes, in the 3 to 10 mL range, for local anesthetic, contrast, and injectate must be provided. To prevent needle movement during attachment of multiple syringes to the needle hub after optimal needle position is obtained, a small-bore, low-volume extension tube can be of great help. These are available in various lengths (3 to 30 inches), and volumes (0.23 to 0.5 mL), depending on operator preference. Extension tubing also allows the physician to keep his/her hands out of the x-ray beam during injection of contrast using active fluoroscopy as mandated for safety. Medications Local anesthetics are used in nearly all spinal injections. A comprehensive review of these medications is beyond the scope of this chapter and can be found in a vast number of anesthesia references. Amide type local anesthetics (lidocaine and bupivacaine) are the preferred choice, have an extremely safe profile when compared to the ester-based (procaine, chloroprocaine and tetracaine) choices. Epinephrine, added 1:100,000 to 1:400,000, increases morbidity and has no use in the practice of pain intervention. True allergic reactions to amide-type local anesthetics are rare, in the range of 1:100,000. Para-aminobenzoic acid (PABA), used as a preservative, or as a metabolic product of the ester-type local anesthetics, can initiate an allergic reaction and their use is, therefore, highly questionable. With the small doses of local anesthetics used in interventional pain procedures, doses capable of causing neurologic or cardiovascular problems should never be encountered. For patient comfort and acceptance, anesthetizing the skin and underlying tissues prior to procedure needle insertion is suggested. Although skin localization may not be required when 25-gauge needles are used, insertion of needles in the 17 to 22 gauge range can be quite uncomfortable. One percent (1%) preservative-free lidocaine, 4 to 5 mL, is ideal for this use. Using a 25-gauge, 1.5-inch needle, excellent conditions for any epidural injection can be easily and safely obtained. Injection of local anesthetic into the epidural space is highly dependent on practitioner practice. Patients are selected, as previously discussed, for radicular-type pain secondary to a proposed inflammatory neuropathology. These patients frequently suffer from chronic complaints. Because local anesthetics provide only

1 to 3 hours of neuroblockade, no long-term relief can be expected from the local anesthetic. However, in a patient who presents in moderate-to-severe pain, even the short relief noted by addition of local anesthetic might warrant its use after the added risk profile is considered. Local anesthetic placed in the epidural space has no positive diagnostic value, whether via the interlaminar or transforaminal route. Nerves are ubiquitous within the epidural space and spread of injectate is nonselective. However, in transforaminal epidural injections, the use of local anesthetic in a concentration high enough to cause sensory block, can provide the physician with reliable negative information. If a patient presents with right lower extremity radicular-type pain, and pathology correlates well with this symptom, a transforaminal injection at the appropriate level would appear to be indicated. In this case, corticosteroid alone might be expected to provide long-term benefit owing to its antiinflammatory action. If the corticosteroid were administered with local anesthetic, and the patient saw excellent relief of preprocedure pain, little inference can be made. However, if the patient saw minimal or no relief and significant numbness in the specific dermatome of the segmental nerve that was targeted, one can make the assumption that the cause of the pain is not associated with that specific level. This is helpful in ruling out this level as associated with the pain generator. Although there are a number of corticosteroids that have been used epidurally by interventional pain physicians for more than 50 years, none have been approved for intraspinal use by the United States Food and Drug Administration (FDA). All corticosteroids must, therefore, be described as “off label.” Methylprednisolone, betamethasone, triamcinolone, and dexamethasone have all been advocated. Of the aforementioned corticosteroids, the first three are suspensions, only dexamethasone is a solution that is commercially available.117 Regarding transforaminal injections, there appears to be correlation between the use of particulates and spinal cord and brain infarctions owing to arterial occlusion. Therefore, for cervical, thoracic, or lumbar injections into the intervertebral foramen, the solution, dexamethasone, would appear to offer a real safety benefit. The use of nonionic, water soluble contrast media is mandated for all fluoroscopically guided spinal injections. Iohexol (Omnipaque) or iopamidol (Isovue) in concentrations of 180 to 300 mg/mL are safe—with allergic reactions occurring in the 1:100,000 to 1:500,000 range. Injection of contrast validates that the needle is in correct position and that the active injectate will cover the targeted anatomic structure. In addition, the pattern of contrast will ensure that the needle tip has not unintentionally strayed into a position where injection might cause significant morbidity. Training in “normal,” aberrant, and potentially dangerous contrast patterns is essential. Although emergent situations are rare during the practice of interventional pain procedures, vigilance and preparedness are essential. One never knows when a situation requiring immediate intervention will occur. Physicians performing spinal injections must be proficient in emergency protocols including airway management and cardiovascular resuscitation. A basic course such as Advanced Cardiac Life Support (ACLS) should be considered a minimum requirement. In addition, well-trained, and practiced, procedure room personnel who are able to assist the physician and monitor the patient provide a safeguard to ensure immediate and appropriate patient care, should the unexpected occur. Whether the procedure is performed in an office, ambulatory surgery center, or hospital setting, emergency equipment, pharmaceuticals, oxygen, airway supplies,

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suction, and other resuscitation provisions must be immediately available and checked regularly to ensure proper function. Monitoring devices such as pulse oximetry, noninvasive blood pressure, and ECG, must at the least be immediately available, and their use is required if any sedation is contemplated. An ongoing conversation with the patient is always an appropriate and accurate monitor of the patient’s comfort, level of consciousness, cardiac and respiratory status pre-, peri-, and postprocedure.

Intravenous Access IV access should not be considered mandatory for routine injections of steroid into the epidural space, be it cervical, thoracic, lumbar, or sacral. Although some medical facilities mandate an IV, and at least one well respected guideline concerning spinal injections (ISIS) recommends the practice for transforaminal injections,118 it should not be considered standard of care. Although complications requiring the use of IV medications, (allergic reactions, severe vasovagal reactions, high intrathecal-spinal anesthetic block) are exceedingly rare, the high cost and risk/benefit ratio make routine intravenous cannulation questionable. Of course, use of sedation requires intravenous access.

Sedation The administration of corticosteroids into the epidural space is minimally painful and the use of sedatives, hypnotics, amnestics, and analgesics is rarely medically indicated. Rather than by medical necessity, the use of these medications is more often governed by patient expectations of a completely pain-free procedure and physician intolerance of any patient movement or interaction during the procedure, and varies significantly from region to region within the country. If sedation is used, intravenous access is obviously required (except when only mild oral medications are given). Although light sedation may have a place in the markedly anxious patient, when carried to a point where the patient is unresponsive or minimally responsive to a painful stimulus, it must be considered dangerous and is never appropriate for epidural injections at any level or with any technique. At all times during the course of the procedure, the patient must be able to converse with the attending physician. If not obtunded prior to any untoward event, the patient will often give a vocal warning of unintentional misplacement of the needle. Unfortunately in many instances, sedation is used to conceal poor operator technique. Sedation can never take the place of technical competence. One often overlooked aspect concerning the use of sedation in minimally painful procedures is the expectation created by their use, and the validation of complaints elicited from the patient. Routine use of sedation creates in the patient the presumption that the planned procedure is inherently excruciating to such a degree that sedation is required; this belief is self-fulfilling. In addition, the psychological overlay, often seen as a comorbid condition in the chronic pain patient, validates the patient’s idea of the extreme severity of the condition, because a procedure that requires sedation must be serious. In competent hands, the optimum sedation is often attained by providing the patient with a detailed account of the anticipated procedure during the consent phase of the interaction, “talking the patient through” the procedure, for example, ensuring that he/she is aware prior to any sensory stimulation, engaging the patient in conversation, and perhaps using music, or other sensory stimulation, as a mild distraction.

Preparation and Drapes When aseptic precautions are used, infection following epidural administration of corticosteroids is quite rare. The skin at, and around, the point of needle insertion is prepared using an iodinebased solution (e.g., povidone-iodine), or chlorhexidine, with or without alcohol, followed by sterile towels or fenestrated drapes to cordon off the area. A change in level or procedure, might be necessary because of unforeseen events, or individual anatomic variation or pathology and a larger skin “prep” than anticipated is never disadvantageous. Sterile technique is mandated throughout the procedure.

Periprocedure Techniques Caudal Needle Placement Caudal injection (i.e., access to the epidural space via the sacral hiatus) has been largely replaced by the slightly more selective, precise interlaminar and highly selective transforaminal approaches. However, if the practitioner’s training is questionable, L5 or S1 bilateral symptomatology is noted, or anatomic considerations prevent the use of other epidural approaches, a caudal injection might be entertained. Entry into the caudal canal involves needle placement though the sacral coccygeal ligament. Traditionally, this was accomplished by palpation of the sacral cornu and placement of the needle blindly. As documented previously, an unacceptably large percentage (>30%) of these injections failed to reach the caudal canal and nonfluoroscopically guided injections are no longer an acceptable routine practice. Caudal injections involve injectate being deposited between the S3-4 levels, with rostral spread hopefully reaching the pain generator two to four levels above, depending on needle tip location within the sacral canal. This injection at a distance may necessitate the use of a larger volume of injectate with reduced concentration of corticosteroid. The patient is placed in the prone position (often a pillow under the hips provides increased access). Rotating the feet so that the toes are pointed medially and the heels lateral will relax the gluteal muscles and facilitate access to the entry point. In obese patients with large buttocks and a deep gluteal cleft, 3-inch surgical tape can be used to pull the buttocks apart and allow access to the needle insertion area over, or somewhat caudal, to the sacral cornu. The skin over the sacral hiatus, including the lower lumbar and sacral areas, is prepared and draped sterilely. The fluoroscope is positioned in lateral view because the sacral hiatus is usually quite difficult to identify using an anteroposterior (AP) fluoroscopic orientation. In a lateral view, the sacral lamina can be seen to extend down to S4 with an abrupt drop off noted identifying the sacral hiatus (Fig. 35-1, A). A metal pointer is positioned in the midline, over or slightly caudal to the sacral hiatus (see Fig. 35-1, B) and a 25-gauge needle is inserted (see Fig. 35-1, C). Anatomy allows the use of a 1.5-inch needle in the majority of cases. The needle will be felt to puncture the sacral coccygeal ligament and contact with os will be noted at the dorsal aspect of the S4 vertebral body in the ventral caudal canal. If the injectionist desires to advance the needle cephalad, a slightly more caudal insertion might be used. In this case, the needle can be advanced up the caudal canal to the level of S3—the level to which the dura extends in most individuals. When the needle is in position, contrast is injected under real time fluoroscopy. DSI (Fig. 35-2, A and B) often provides a more exact indication of the rostral contrast spread. Ventral flow through the ventral sacral foramen is often seen and can be extensive 

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Figure 35-1  Lateral view of the sacrum. A, Arrows indicate extent of sacral hiatus. B, Pointer on skin at midline indicates needle insertion point over sacral hiatus. C, Needle in place penetrating sacral coccygeal ligament and contacting the dorsal S5 vertebral body.

(see Fig. 35-2, C). Although an AP image is often obtained, the flow of contrast is usually better appreciated in the lateral view as is unintentional dural puncture. If appropriate spread of contrast is appreciated, the corticosteroid preparation with normal saline, 3 to 5 mL total is injected. Three milliliters of injectate will reach the L5-S1 disc level in approximately 80% of the injections (see Fig. 35-2,  D). Larger volumes provide little added benefit. The extra epidural flow, as noted earlier, can severely limit the volume of active injectate actually reaching the pain generator (Fig. 35-3). Images documenting needle position prior to injection, and verifying contrast pattern and extent of coverage, must be saved for the medical record. Lumbar Interlaminar Because lumbar interlaminar (i.e., between the lamina) epidural injections place the active injectate closer to the area of pathology, they must be considered somewhat more selective than caudal administration of corticosteroids. These injections are often mislabeled as “translaminar,” that is, through the lamina. The needle is placed into the epidural space via a posterior approach, through the interlaminar space, and ligamentum flavum, but stopped prior to dural puncture. Injection is made into the dorsal epidural space (Fig. 35-4). Interlaminar lumbar epidural injections of corticosteroid are the most often performed interventional pain procedure, even though their efficacy is questioned by many practitioners who are intimately involved with the discipline. Although most physicians within the specialty have patients who claim relief from these injections, interlaminar injections might be considered as “frequently performed procedures of unvalidated value.” However, interlaminar epidural injections performed with the use of fluoroscopy and targeted to level and side of pathology cannot be considered equivalent to the blind, nonvalidated injections of yore. The patient is positioned prone, with a pillow under the abdomen to decrease the anatomic lordotic curve. Often with obese patients, the large abdomen will provide the proper anatomic position

without additional padding. Placing the patient in sitting position where a fluoroscope is used in lateral view only, provides no benefit, has technical limitations, must be considered a bastardization of the technique taught to anesthesia residents, and indicates lack of training, understanding, and proficiency with the use of a fluoroscope for spinal injections. Although one wishes to place the needle in proximity to the underlying pathology, injectate of even a small volume will spread over several levels. Injectate placed within the epidural space in the midline dorsal position, will take the path of least resistance and may never reach the ventral aspect of the epidural space where the pain generator in the form of disc deformity or stenosis is found. However, if placement of the needle toward the side of complaint/ pathology, and bevel control is used, contrast can be seen flowing to the ventral aspect of the epidural space and the intervertebral foramen, and the nerve root canals can be clearly identified. Following appropriate positioning, the lumbosacral region is prepared and draped sterilely. The fluoroscope is used to examine the lumbar spine. Segmental anomalies such as sacralized L5 vertebral bodies, or nonsacralization of S1 should be noted and detailed on the procedure note. The targeted interlaminar space is then identified in an AP view (Fig. 35-5, A) caudal to the pathology unless a far lateral needle placement is contemplated. Because the majority of pathology is seen in the two lower lumbar levels, the L5-S1 and L4-5 interlaminar spaces are the most frequent targets. Cephalocaudal tilt results in the interlaminar space being seen at its maximum size, whereas a slight ipsilateral oblique view often provides easier access. When adequate visualization is obtained, the skin over the target is marked (see Fig. 35-5, B). Local anesthetic can then be injected (see Fig. 35-5, C) and the epidural procedure needle advanced. At this point, tactile feel is of utmost importance and can only be taught using “hands on” instruction in living subjects. The needle is felt to transverse through the various tissue layers until a midprocedure position is noted; resistance to needle advancement is noted secondary to contact with the ligamentum flavum (see Figs. 35-5, D and Fig. 35-6, A). Although some experienced

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practitioners make a point of contacting os on the superior aspect of the lamina caudal to the targeted space, the feel of contact with ligamentum flavum, is as distinct as this boney target. If contact with bone was sought, and contact was made, the needle is slightly withdrawn, redirected, and advanced until the distinct resistance of ligamentum flavum is noted. At times, insistence on contacting os prevents targeting a specific area of the interlaminar space. If os is not touched, the ligamentum flavum is engaged directly. Using a loss of resistance (LOR) technique with either constant pressure on the plunger of a glass/plastic LOR syringe with normal saline or short interval, light intermittent pressure with an air-filled LOR syringe, the needle is advanced. A very obvious loss of resistance to the saline or air is noted as the needle aperture exits the ventral

aspect of the ligamentum flavum and enters the epidural space. At the present time, hanging drop and Macintosh balloons must be considered passé and of historical interest only. A lateral view can now be used to indicate needle depth (see Fig. 35-6, B) if necessary. However, if the needle is not placed in the exact midline, or a “true lateral” is not used, depth as noted by visual clues can be faulty due to the tangential imaging. No specific bony landmarks are available to verify needle tip entry into the epidural space. Special care must be taken when working above the L2-3 level because the spinal cord must be considered. Aspiration, at this point, should evidence no or very minimal, clear or lightly blood-tinged fluid. As noted earlier, with the use of small needles, CSF return is not a reliable indicator of

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Figure 35-2  Lateral view of the sacrum. A, Digital subtraction imaging (DSI) at start of contrast injection. B, DSI at conclusion of contrast injection. Open arrows indicate extent of contrast within caudal canal. Black arrows indicate contrast flow through S2 and S4 ventral foramen. C, Lateral view at conclusion of contrast injection. Open arrows indicate extent of contrast within caudal canal. Solid arrows indicate contrast flow through S2 and S4 ventral foramen. D, Lateral view lumbosacral junction. Contrast is seen up to the L5 pedicle.

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intrathecal needle placement. Images to document placement in AP, and possibly lateral views are obtained (see Figs. 35-6, B and 35-7, A). Injection of contrast, under active fluoroscopy in AP view is now performed to ensure needle position by contrast pattern (see Fig. 35-7, B-F). A nonhomogeneous, vacuolated pattern is apparent with epidural injection versus the homogeneous pattern noted with injection into the CSF. Although an AP view may make noting an intrathecal injection difficult, vascular uptake will be obvious because these structures are perpendicular to the needle, and visualization is transient owing to flow within the structure. A lateral view is now used to rule out intrathecal or subdural patterns

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Figure 35-3  Anterior-posterior (AP) view of lumbosacral junction. Note partially sacralized L5 vertebral body on left. White arrows indicate extent of contrast within caudal canal. Black arrows indicate contrast flow through S1, S2, and S4 ventral foramen.

and verify epidural spread of contrast in the dorsal epidural space  (Fig. 35-8). Subdural injections between the dural and arachnoid layers will be cystic with clearly delineated margins. Subarachnoid  injections of contrast in the lateral view will layer out in the ventral intrathecal space because it is heavier than CSF. Subdural injections mandate withdrawal of the needle dorsal to the liga-mentum flavum and reinserting toward a different target with LOR once again appreciated. If dural puncture is noted with an intrathecal pattern, the procedure can be attempted at an adjacent level or abandoned for that day. After validation of epidural injection is obtained and images are saved, the physician can now proceed with the injection of corticosteroid in a total volume of 2 to 4 mL. Larger volumes will result in wider dispersion of a less concentrated mixture, neither of which factors is beneficial if a specific pathology has been targeted. A socalled “washout” or postinjection film can be saved to document final dispersion of material within the epidural space (Fig. 35-9). Because one is often treating a unilateral, or one side dominant, pain complaint, one of the authors (ML) targets the side of pathology/symptomatology. Fig. 35-10) illustrates this alternative approach where flow into the ventral epidural space and segmental nerve canals is routinely observed with a proposed increase in efficacy. Normal saline or local anesthetic can be used as the diluents with corticosteroid, realizing that local anesthetic provides no diagnostic information and adds significantly to the morbidity profile without added therapeutic value and requires a lengthier postprocedure monitoring period. Because no arterial structures are present in the epidural space that could lead to catastrophic complications, a particulate corticosteroid is not contraindicated for this procedure. Mild transient low back pressure or a mild transient pressure paresthesia may be experienced by the patient. This is often concordant with the patient’s usual pain complaint and does not require discontinuance of the procedure, unless the pain is severe. Thoracic Interlaminar The thoracic interlaminar technique involves additional risks because the spinal cord lies millimeters ventral to the ligamentum flavum. In addition, the dorsal epidural space is narrower than in the lumbar region (Fig. 35-11). This procedure should not be attempted

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Figure 35-4  A, MRI axial T1 WI at L4-5. Arrow indicates needle track into epidural space. B, MRI sagittal T2 WI with arrows pointing to epidural space at L4-5 and L5-S1.

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Figure 35-5  Anteroposterior (AP) image at lumbosacral junction. A, L5-S1 interlaminar space indicated by arrows. Note end plates of the L5-S1 disc are not parallel to beam to maximize interlaminar space (i.e., the target). B, Pointer indicates site of skin entry over target. C, Track of local anesthetic injected as a 25-gauge, 1.5-inch needle is withdrawn. D, 18-gauge epidural needle meeting resistance from ligamentum flavum.

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Figure 35-6  Lateral image at ­lumbosacral junction. A, Needle is touching ligamentum flavum as noted by resistance to further ­advancement. Arrow indicates needle tip. B, Needle has been advanced through ­ligamentum flavum with loss of resistance to saline noted as tip (arrow) enters epidural space.

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Figure 35-7  Anteroposterior (AP) image at lumbosacral junction during injection of contrast. A, Needle is positioned in epidural space prior to injection of contrast. B, Digital subtraction imaging (DSI) at start of contrast injection. C, DSI at midinjection. Note development of nonhomogeneous, vacuolated pattern typical of epidural spread. D, Toward end of contrast injection. Note midline, spreading, nonhomogeneous, vacuolated pattern typical of epidural contrast. E, DSI and F, plain fluoroscopy, at end of contrast injection approximately 2.5 mL of contrast. Note midline, nonhomogeneous, vacuolated pattern typical of epidural spread. S1 nerve canals clearly identified, solid black arrows. Contrast beginning to outline the right L5 nerve root canal, open arrows. White arrows indicate rostral spread of contrast.

by any physician who has not had extensive training and experience working in the lumbar region. As with all interlaminar injections, the patient is best placed in a prone position and an appropriate sterile preparation of the skin and draping at the proposed skin entry site are completed. Because the lamina of the thoracic spine resemble overlapping shingles on a roof, excellent visualization of the interlaminar space is often impossible. Anatomically, the interlaminar space will always be found ventral to the spinous process of the rostral level. Using the fluoroscope, the targeted interlaminar space is identified and optimum visualization is obtained using cephalocaudal tilt of the image intensifier (Fig. 35-12, A). A  paramedical approach is advocated because the orientation of the lamina and spinous process often makes a midline approach difficult, especially if any degree of rotoscoliosis is present. This becomes quite evident in the midthoracic region, T4-10.

Using an AP orientation with caudal tilt of the image intensifier, the skin entry point is marked, slightly more than one level below the target and lateral to midline (see Fig. 35-12, B). Therefore if the T10-11 interspace is targeted, the skin entry would be over the T12 lamina. A local anesthetic track toward the lamina above is completed to a depth of ~1.5 inches. The epidural needle is advanced toward the targeted midline interlaminar space and os is contacted over the lamina (T11) of the vertebra just caudal and lateral to the target (see Fig. 35-12, C). The needle is then slightly withdrawn and advanced slowly toward the spinous process rostral to the target (T10). The distinctive resistance of the ligamentum flavum will be noted and advancement of the needle is halted. A lateral view may be obtained at this point and the needle tip will be noted lying dorsal to the epidural space. Using the LOR technique as described earlier, the needle is advanced slowly through the ligamentum flavum.

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Figure 35-8  Lateral image at lumbosacral junction at end of contrast injection. Note spread in dorsal epidural space with minimal contrast identified ventrally. L5 and S1 segmental nerves identified, black arrows. White arrows denote spread of contrast between L4 and S1 emphasizing the nonselective nature of interlaminar injections.

Figure 35-9  Anteroposterior (AP) “washout” image at lumbosacral junction after injection of 3 mL corticosteroid and normal saline. L5 and S1 ­segmental nerves identified (black arrows). Spread of contrast between L4 and S2 emphasizing the nonselective nature of interlaminar injections (white arrows).

It is important to realize that the anatomy of the thoracic spine differs from that of the lumbar spine in that the transverse processes angle to a greater extent dorsally, and the superior articular processes (SAP) lie ventral to their anatomic position in the lumbar spine. The needle, when within the dorsal thoracic epidural space, will appear dorsal to the lamina and SAP (see Fig. 35-12, D). Images precontrast, AP, and lateral, to document needle position are archived. After negative aspiration for CSF and blood, contrast is injected and flow is verified in the dorsal epidural space (Figs. 35-13 and 35-14). Because of the narrowness of the epidural space in the thoracic spine, spread of a small volume of contrast can be extensive with 2 to 3 mL covering greater than five levels with flow to the ventral spinal canal being minimal  (see Fig. 35-14). When epidural placement of the needle is verified, the corticosteroid of choice can be injected using a diluent of either normal saline or local anesthetic. Volumes of greater than 3 mL are rarely required. Mild, transient dorsal pressure is often experienced by the patient. As with any injection into the epidural space, no validated positive diagnostic value can be ascertained whether or not local anesthetic is used.

received, proper technique is used, care and vigilance is practiced, and significant, extensive experience at other levels is obtained prior to attempt of this seemingly easy procedure. The cervical epidural space is narrow, 3 to 5 mm, and the tactile clues differ significantly from the lumbar or thoracic levels. The anatomy is unique especially in regard to the dorsal angle of the laminae, presenting imaging uncertainty when assessing depth within the central canal. In patients with short necks or large body habitus the shoulders may prevent adequate lateral visualization at C7-T1 or even C6-7. In addition to the anatomic variation, knowing that only millimeters separates an injection into the dorsal epidural space from penetration of, and injection into the spinal cord, creates an apprehension knowing that death or quadriplegia can easily result from a slight needle misadventure. Prior to any placement of a needle into the cervical canal, a recent high quality MRI or CT scan must be evaluated by the physician planning the injection (Fig. 35-15). Canal diameter must be assessed prior to the injection to ensure adequate space within the epidural space. The epidural space must be assessed to see if an interlaminar injection can be performed safely. The normal diameter of the spinal canal is 12.5 mm or greater, with a cord diameter of ~9 mm. Cerebral spinal fluid (CSF) should be identified surrounding the cord on axial views. An AP diameter of less than 11 mm is considered to be relative spinal stenosis, whether congenital (i.e., owing to short pedicles) or secondary to acquired pathology (i.e., disc protrusion or spondylosis). An AP diameter of less than 10 mm is significant and placement of a needle at any level with this degree of compromise, is questionable, especially if no epidural fat is noted dorsally on imaging. Because the dorsal epidural space thins markedly above C6, interlaminar injections above the C6-7 level are never appropriate and pose an undue risk to the patient. Dr. Richard Derby, an outstanding, experienced, and well known interventional pain physician from an anesthesia background, stated that, “a cervical epidural

Cervical Interlaminar

…one forgets the tiger heart that pants beneath it; and would not willingly remember, that this velvet paw but ­conceals a remorseless fang. Herman Melville Interlaminar injections may appear elementary in the hands of an expert, but significant morbidity and mortality has occurred when the inexperienced injectionist has not heeded the aforementioned advice. Access to the cervical epidural space via the transflaval approach can be accomplished safely if quality instruction is

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Figure 35-11  MRI thoracic spine axial T2 WI. Arrow indicates dorsal epidural space.

Figure 35-10  AP image at lumbosacral junction. A, Needle is in epidural space as noted by loss of resistance to saline. Note far lateral needle placement under lamina. B, Digital subtraction imaging (DSI) and C, plain fluoroscopic images of the lumbosacral junction at completion of contrast injection. Right unilateral epidural contrast pattern with L5 and S1 segmental nerve canals clearly identified (black arrows). D, Lateral “washout” image at lumbosacral junction following contrast and 3 mL injection of corticosteroid and normal saline. Contrast is clearly evident in the ventral epidural space and L4, L5, and S1 segmental nerves are identified (arrows).

injection rarely should be performed above C7-T1.”119 Because the most common levels of pathology occur at C5-6 or C6-7, this makes the C7-T1 interlaminar spaces ideal to target. If pathology, anatomy, or postsurgical changes necessitate, the T1-2 interlaminar space can be chosen. In a series of patients by one of the authors (CA), CT scan approximately 15 minutes post-interlaminar injection, using small volumes at the lower cervicothoracic junction, has shown contrast covering the entire cervical epidural space. Therefore, precision of level might be a moot point and of little significance regarding cervical interlaminar injections. The patient is placed in the prone position with the neck slightly flexed. The posterior upper dorsal and cervical regions are prepped and draped in a sterile manner. The AP fluoroscopic view is obtained (Fig. 35-16, A) and the targeted interlaminar space identified. Using cephalocaudal tilt, the image intensifier is positioned to maximize the interlaminar space (see Fig. 35-16, B). In most cases, a slight paramedian approach provides the easiest access, and a slight ipsilateral oblique view may be helpful. Some practitioners advocate a midline approach, perpendicular to the ligamentum flavum and the dorsal dura. However, the feel of the needle contacting and traversing the ligamentum flavum is an important

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technical aspect of this procedure. Because the resistance noted by contact with the ligamentum flavum is correlated to the distance traversed through it, this resistance is increased when entering at any decreasing angle from perpendicular to this structure. In addition, needle contact with the dura at a 90-degree angle is more apt to result in trespass into the intrathecal space, with subarachnoid injection, or cord penetration. Dural contact at a less acute angle would be expected to distort or “tent” the dura without penetration, with fewer expected cases of intrathecal encroachment. The LOR technique with saline will increase this “dural tenting” because a low-volume stream of pressurized saline will be injected into the potential epidural space before extensive needle entry, distorting the dura and providing some additional space and margin of safety. Therefore, a paramedian approach (Fig. 35-17) with a LOR technique with saline, might be considered a safer alternative. Using the paramedian approach, a point on the skin is marked lateral to midline over the superior lamina of the level below (Fig. 35-18, A) and local anesthetic is injected (see Fig. 35-18, B). Care must be used because the average depth from skin to epidural space

Figure 35-12  AP image of thoracic spine. A, T10-11 interlaminar space is noted by dark arrow. B, Pointer marking needle skin entry for T10-11 interlaminar epidural needle placement, paramedian and one level below target. C, Loss of resistance has indicated needle tip as having entered the epidural space. Arrow indicates position of needle tip when lamina first contacted. D, Lateral image of thoracic spine. LOR has indicated needle tip as having entered the epidural space. Note tip of needle appears dorsal to posterior elements (double-headed arrow), indicating that tactile information and experience alone, versus visual clues, are of paramount importance in the performance of this injection.

at C6-7 and C7-T1 is 57 mm (2.25 inches) and 54 mm (2.12 inches) at T1-2120, in an exceedingly slender person a 1.5 inch needle might be long enough to reach the spinal canal with intrathecal injection of local anesthetic resulting in a “high spinal block,” or spinal cord injection. The epidural needle is then advanced through the anesthetized tissue toward one of two endpoints. Many practition­ers advocate contact with the most rostral aspect of the lamina to provide a reliable measure of depth (see Fig. 35-18, C). However, if this bony contact cue is missed due to imaging uncertainty or inexperience, the injectionist while expecting this firm contact with os, might unknowlingly advance the needle through the ligamentum flavum, dura, and into the spinal cord. When os is contacted, a lateral view can be obtained and depth can be verified as dorsal to the spinolaminar line. The needle is then slightly withdrawn, redirected to slide off os, and the ligamentum flavum is contacted. A more experienced physician, who has gained a tactile sense of the needle passing through distinctive tissue layers, may omit the touching of the lamina and advance the needle directly toward the interlaminar space until the distinct feel of the ligamentum flavum is noted.

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Figure 35-13  AP images of thoracic spine with needle in epidural space. A, Plain fluoroscopic image prior to contrast injection. B-D, Sequential series of digital subtraction imaging (DSI) during contrast injection. Note wide spread of contrast and vacuolated epidural pattern typical of a thoracic epidural injection. B, Beginning of contrast injection, volume ~0.75 mL. C, Midinjection. Volume ~1.75 mL. D, End of contrast injection, volume ~2.5 mL. Note wide spread of contrast (arrows) and vacuolated epidural pattern typical of a thoracic epidural injection. E, Plain x-ray image at end of injection. Approximate volume 2.5 mL. Note wide spread of contrast (arrows), and vacuolated epidural pattern typical of a thoracic epidural injection.

When the ligamentum flavum is contacted, the LOR syringe is attached and the needle is slowly advanced until loss of resistance with saline or air, as described earlier, is noted (see Fig. 35-18, D). A quasi feel of loss of resistance is often present in the cervical spine as the needle transverses the tissue between the interspinous ligament and ligamentum flavum, and only experience may be able to differentiate this from the “true” loss of resistance as one enters the epidural space. In addition, a false loss of resistance can also be appreciated when in close proximity to periosteum prior to the tactile sensation of laminar os being contacted. When the needle has traversed the ligamentum flavum and is in the epidural space (see Fig. 35-18, E) aspiration should be negative for CSF and blood. If CSF is noted, the needle must be withdrawn and either epidural placement attempted at a different level or, possibly a better option,

the procedure discontinued and the patient discharged to return at a future date. If frank blood is noted, the needle is withdrawn dorsal to the ligamentum flavum is redirected, and loss of resistance is once again sought at a slightly different area. Although a true lateral view with identification of the needle at the spinolaminar line has been advocated to verify depth prior to injection of contrast, this technique can be fraught with misleading information (see Fig. 35-18,  F). A single lateral view is not sufficient to gauge depth because the laminae in the cervical spine are not orthogonal, perpendicular to the x-ray beam; they slope at approximately 45 degrees (see Fig. 35-19). Lateral images are further distorted secondary to the displacement of the needle tip from midline. For every aberration, the lateral image becomes progressively less valid. To exactly calculate needle tip position,

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the AP view provides information about the rostral-caudal and medial-lateral placement, whereas a tangential image through the lamina opposite which the tip of the needle lies (i.e., the contralateral oblique view) delineates needle depth—although being dependent on the precise degree of obliquity can be deceptive as to the

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Figure 35-14  Lateral image of thoracic spine at end of injection. Approximate volume 2.5 mL. Note dorsal epidural pattern and wide spread of contrast (arrows) covering levels typical of a thoracic epidural injection.

reality of needle tip position. Exact knowledge of needle placement requires tactile clues as to tissues penetrated, multiple fluoroscopic views, and the training, experience, and expertise to evaluate each unique situation. Unlike many other injections, two views, AP and lateral, do not always provide sufficient information to accurately place the tip of the needle in a safe position. All images indicating that the needle is in a safe final position, prior to contrast injection, are archived. When access to the epidural space is evidenced through the use of LOR and possibly by imaging, contrast is injected under active fluoroscopy (see Figs. 35-20 to 35-23) in a volume that will ensure that the injection is being made within the epidural space, and that intrathecal, subdural, and vascular flow are absent. A volume of 2 to 3 mL is usually adequate. Images of contrast verifying safe needle position and appropriate contrast flow are saved for the historical record. Verification of needle position with contrast is followed by injection of the active pharmaceutical compound, corticosteroid. Diluents of either normal saline or low concentration local anesthetic can be used safely with the understanding that neither has a therapeutic or diagnostic role and local anesthetic can be assumed to have a higher morbidity profile. As in the lumbar region, the patients chief complaint, and index pain is often unilateral or one-side dominant. Again, one of the authors (ML) feels compelled to target the side of pathology/ symptomatology, especially when as noted, a less than perpendicular approach to the epidural space may provide a margin of safety as the anatomy in Figure 35-17 indicates. Figs. 35-22 and 35-23 illustrate this alternative approach where flow into the ventral epidural space and segmental nerve canals is routinely observed with a theoretical increase in efficacy. During injection, it is common for the patient to note some neck pain as well as transient, mild pressure paresthesia into the

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Figure 35-15  A, MRI sagittal T2 WI at midline. Note minimal epidural space at C6-7 (black arrow); increasing at C7-T1(white arrow); “large” at T2-3 (open arrow). A small protrusion is noted at C6-7. B. MRI axial T2 WI at C7-T1. Black arrow points to the epidural space. Double headed arrow indicates an adequate sagittal spinal canal diameter with cerebrospinal fluid (CSF) noted surrounding the cord.

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Figure 35-16  A, Scout AP view cervicothoracic spine. B, Slight right oblique view cervicothoracic spine. Arrow indicates maximized C6-7 interlaminar space.

Figure 35-17  MRI axial T2 WI at C7-T1. A needle path from a left paramedian approach to midline (black solid arrow) if inadvertently advanced will puncture the dura and enter the spinal cord. However, a needle targeting a lateral target within the epidural space (white broken arrow) will possibly miss the cord if overly advanced and may never puncture dura.

upper extremity, in addition to a feeling of “warmth” and “pressure,” in the chest. These symptoms do not necessitate discontinuing the injection unless they are severe.

Transforaminal Injections versus Selective Spinal Nerve Blocks Corticosteroids placed into the epidural space via the intervertebral foramina are often described as selective spinal nerve blocks. This is a gross misunderstanding of the anatomy involved and the rationale behind the procedure. The target of the injection is the

pain generator, known in the case of radicular pain to be the dorsal root ganglion (DRG), and the associated pathology being deformity of the outer intervertebral disc margin (i.e., protrusion, extrusion, sequestration, or spinal stenosis.) These pathologies usually involve the medial aspect of the foramen and/or spinal canal. Therefore, for the active injectate to be of benefit, it must flow through the foramen into the epidural space. Corticosteroids are antiinflamatory medications and the intent is not to “block” neural transmission. The local anesthetic, neural blocker, often used as part of the injection is not therapeutic and is merely “along for the ride,” although it might provide negative diagnostic information, and validate the corticosteroid as having been placed in close proximity to the pain generator. The fact that epidural spread is desired (whether or not local anesthetic is used) invalidates the concept of “selective” because any medication placed within the epidural space is in contact with multiple neural structures and is, by definition, nonselective. Even the concept of a “selective epidural” must be considered a gross misrepresentation of the procedure and a failure to understand the pertinent anatomy. Selective spinal nerve blocks (SSNB), are injections into the foramen, with an extremely small volume, 0.3 to 0.5 mL, of concentrated local anesthetic (e.g., lidocaine 4%). They are at best a “quasidiagnostic procedure” which is neither selective nor validated as diagnostic. If limited to the foramen, questions about the level of symptomatology might be addressed. Because neural structures within the intervertebral foramen include the dorsal root ganglion, spinal nerve, dorsal ramus, medial branch, intermediate branch, lateral branch, ventral ramus, sinuvertebral nerve, and gray ramus communicans, local anesthetic limited to the foramen can hardly be called “selective” in any sense of the word, and is of limited positive diagnostic use.

S1 Transforaminal Corticosteroid Injection Technique Of the lumbar intervertebral discs, L5-S1 is the second most common to suffer from protrusion, or extrusion, often with S1 segmental nerve involvement. Therefore, instillation of corticosteroid around

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Figure 35-18  A-D, Slight ipsilateral oblique view cervical spine. C6-7 interlaminar space maximized. A, Pointer on skin over target indicating rostral aspect of the C7 lamina caudal and slightly lateral to interlaminar space. B, Needle placement for local anesthetic injection. C, Epidural needle advanced and touching lamina below and lateral to interlaminar space target. D, Needle through ligamentum flavum, verified by loss of resistance to saline and air. Negative aspiration for cerebrospinal fluid (CSF) and blood. E, AP view cervical spine. Needle in epidural space at dorsal midline. F, Not true lateral view cervical spine. Note margins of neural arch not aligned (arrows). Needle appears somewhat ventral to spinolaminar line (broken line) due to suboptimal imaging. Compare to Figure 35-21, A.

the S1 DRG is a procedure frequently employed by the interventional pain physician and constitutes one of the core procedures of our specialty. This injection requires placing a needle through the dorsal foramen of S1, thereby accessing the S1 nerve canal. The patient is placed in a prone position. The lower lumbar and sacral areas are prepared and draped as detailed previously. Using an AP view, the fluoroscope is oriented to identify the area just caudal to the S1 pedicle on the symptomatic side (Fig. 35-24,  A). The superior end plate of S1 is squared (see Fig. 35-24, B) and a slight ipsilateral obliquity is used until the dorsal foramen is visualized directly caudal to the S1 pedicle and medial to the lateral wall of the S1 nerve canal (Fig. 35-24). The target should be seen as distinct from and slightly rostral to the larger, and often more obvious, S1 ventral foramen (see Fig. 35-25, A and B). The skin entry point is marked over, or just caudal to the target, Fig. 35-26, A, and if desired local anesthetic injected. A 25- or 22-gauge spinal needle is then advanced toward the lateral-­caudal aspect of the foramen (Fig. 35-26, B), just medial to

the lateral nerve canal wall in that the course of the S1 segmental nerve is medial (see Fig. 35-26, B). Slight reduction in resistance to needle insertion will be felt as the needle enters the foramen. As the needle is advanced, it may contact the lateral wall of the nerve canal or the dorsal aspect of the S1 vertebral body (i.e., the ventral canal). The bent needle technique will allow continued precise advancement. A lateral view is used to note appropriate depth with the needle tip lying between the lamina and anterior canal (see Fig. 35-26, C). At this point, AP and lateral images are saved for the permanent medical record to document needle position prior to injection of contrast. Using an AP view, contrast is injected slowly under active fluoroscopy, with DSI if available (Fig. 35-27, A-F). The contrast should be flow proximally toward the L5-S1 intervertebral disc without significant vascular uptake. Although medullary arteries are not seen at this level,121 retrograde venous filling toward the conus might be appreciated and would necessitate repositioning of the needle. If the majority of contrast is noted to travel distally through the

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Figure 35-19  MRI axial T2 WI at C7-T1. Solid white lines indicate ~45-degree orientation of the cervical lamina. The solid black arrow represents a needle within the epidural space to the right of midline. White broken lines represent a true lateral fluoroscopic view. Black broken lines represent a contralateral, left, oblique fluoroscopic view. Note distance between the most dorsal epidural space (black dot) and the needle tip.

ventral foramen, the needle should be repositioned until contrast is covers the targeted structure. A lateral view then demonstrates filling of the S1 nerve canal with minimal contrast flowing out of the ventral foramen (see Fig. 35-27, G). Corticosteroid can now be injected with normal saline or local anesthetic. Because particulate corticosteroids have had catastrophic consequences when injected within a neural foramina, solutions are preferable (i.e., dexamethasone 10 to 15 mg). A total volume of 1.5 to 2.0 mL is usually adequate to cover the targeted area. Appropriate volume can be estimated by the previous flow of contrast. When the corticosteroid is mixed with lidocaine ­(Xylocaine) 4%, a concentration that can be depended on to provide sensory blockade is obtained, which can validate that the pain generator was addressed and provide negative diagnostic information.

Lumbar Transforaminal Injection into the lumbar intervertebral foramen with corticoster­oid for radicular pain is of known therapeutic value. Because the L4-5 intervertebral disc is most susceptible to injury, the most common level for this procedure is the L5-S1 foramen, covering the L5 dorsal root ganglion and segmental nerve. Segmental anomalies of sacralized L5 or nonsacralized S1 vertebral bodies occur in approximately 15% of patients, and care must be taken to ensure the correct level is being injected. The targeted foramen can be identified in an AP image by being bounded in a cephalocaudal orientation by the pedicle above and below, and medial to lateral by the medial and lateral pedicular lines. For the majority of cases, positioning of the needle in a subpedicular position, and in the middle foramen in the dorsalventral orientation, is safe, and distances the needle tip from the possible position of the medullary artery (i.e., artery of Adamkiewicz, as discussed earlier). A so-called “retroneural” positioning of the needle has been described122; however, this technique can be considered

a slight variant of the standard technique. Occasionally, because of marked degenerative changes, no access to the foramen is available via the subpedicular approach. In this case, an alternative infraneural technique can be used that targets the caudal ventral aspect of the foramen, and will be described following the standard approach. The patient is placed in prone position with a pillow under the lower abdomen to decrease the lumbar lordotic curve. After a sterile preparation and draping of the skin at the injection site, the fluoroscope is positioned to obtain an AP view with the pedicle shadow bounding the upper aspect of the targeted foramen, in the center of the fluoroscope monitor (Fig. 35-28, A). As in the majority of spinal injections, to obtain a true AP image, cephalocaudal tilt of the image intensifier is used so that the vertebral end plate closest to the target is “squared,” (i.e., the x-ray beam is parallel to the end plate, which appears as a solid line rather than an ovoid structure). In the case of an L5-S1 transforaminal injection this would be the inferior end plate of L5 (see Fig. 35-28, B), for an L4-5 transforaminal injection the inferior end plate of L4, and so on. An ipsilateral oblique projection is now obtained so that the tip of the superior articular process (SAP) of the level below is positioned under the approximate “6 o’clock” position of the pedicle when seen as a clock face. In the case of the L5-S1 transforaminal injection, the fluoroscope is positioned so that the S1 SAP is seen as positioned under the L5 pedicle (see Fig. 35-28, C). Anatomically, if a needle is now advanced into the subpedicular position, and the tip does not stray medial to the rostral tip of the SAP and 6 o’clock position of the pedicle, the spinal canal is safe from trespass. If desired, a skin wheal can be considered, especially if needles greater than 25 gauge are used. The procedure needle is advanced using a downthe-beam, “tunnel vision,” technique toward the inferior aspect of the pedicle shadow (see Fig. 35-28, D). In most cases, a needle of 5 inches is needed to enter the L5-S1 foramen due to the greater depth required secondary to the cephalad tilt of the image intensifier, as required to obtain a true AP at this level. As the needle is advanced, the operator needs to be ever conscious of depth—realizing that os will in all probability be contacted, and to prevent further insertion, at one of four structures: the lamina, SAP, transverse process, or vertebral body. If the three former boney structures are contacted, the bent needle can be used to maneuver around them. If the lamina, SAP, and transverse process are passed, tactile clues will indicate passage through the dorsal leaf of the intertransversarii muscles.  At this point, a lateral view can be used to verify that the needle has entered the foramen (see Fig. 35-28, F). If the needle is advanced so that the dorsal vertebral body is contacted in the ventral foramen, a lateral view will note this and the needle is withdrawn a few millimeters. An AP view will ensure that the needle has not been excessively advanced medially, past the 6  o’clock position of the pedicle, where entry into the dural root sleeve might be expected (Fig. 35-29, A). Lateral and AP views are saved to document final needle position and provide a permanent record of the procedure (see Figs. 35-28, F and Fig. 35-29, A). An AP view is now used for injection of contrast under active fluoroscopy because the structures that present danger, the medullary artery or retrograde flow to the conus, are perpendicular to the beam and will be well visualized. DSI can be used if available, and the operator has been trained in its use, but is not considered standard of care at this juncture. Contrast should be seen to flow medially through the foramen into the epidural space (see Fig. 35-29, B-F). Contrast will often be seen following the medial border of the pedicle spreading toward the intervertebral disc at

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Figure 35-20  Series of AP view cervical spine. A, Needle in epidural space prior to contrast injection. B-E, Sequential digital subtraction imaging (DSI) during contrast injection. B, Early in injection. C, Early midinjection. D, Later at midinjection. E, Contrast with bilateral spread. Note nonhomogeneous vacuolated pattern consistent with epidural injection. F, Fluoroscopic image at end of contrast injection, ~2.5 mL. Contrast evidences bilateral spread. Note nonhomogeneous vacuolated pattern consistent with epidural injection. G, AP view cervical spine with intervertebral disc end plates squared. Image at end of contrast injection, ~2.5 mL. Note nonhomogeneous vacuolated pattern consistent with epidural injection. Spread of contrast is bilateral and extends between C5 and T1 (arrows).

the level above. If the majority of contrast is seen to flow laterally along the ventral ramus, it shows that a significant portion of the injectate will not come in contact with the pathology, and pain generator, one wishes to treat. Repositioning of the needle is then recommended. Minimal venous uptake is not a contradiction to completing the procedure. However, if marked venous flow

is seen, this necessitates repositioning of the needle and reevaluation with contrast. Vascular flow of contrast laterally, or to the contralateral side, can be presumed to be venous, whereas flow to the midline, with or without evidence of cephalad extension, must be considered arterial and the procedure must be terminated. Following

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Figure 35-21  A,True lateral view cervical spine. Compare with figure 35-18, F. Note needle tip at ­spinolaminar line (arrow). Image at end of contrast injection, ~2.5 mL. Note nonhomogeneous ­vacuolated pattern at spinolaminar line consistent with dorsal epidural injection. Spread of contrast is seen ventrally and extends rostral to C4-5. B, Oblique view cervical. Note needle tip at ­spinolaminar line. Image at end of contrast injection, ~2.5 mL. Note nonhomogeneous vacuolated pattern at ­spinolaminar line consistent with dorsal epidural injection. This view is often required when body habitus prevents adequate lateral imaging of the lower cervical levels.

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Figure 35-22  Needle in position at C7-T1 ­following penetration of the ligamentum flavum evidenced by loss of resistance. Far left lateral targeted interlaminar epidural injection. A, AP view. Note needle under the left medial laminar border. B, Lateral view. Note needle tip (arrow) appears to have passed through the spinal canal illustrated by broken lines. Suboptimal image secondary to patient body habitus. C, Right oblique view (i.e., contralateral to needle tip position). Tip of needle (arrow), is positioned at the left ventral laminar line. Lamina (L). D, Left oblique view (i.e., ipsilateral to needle tip [arrow]). Note that needle appears to have transversed the spinal canal and is ventral to the right ventral laminar line.

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Figure 35-23  Cervical spine after injection of contrast, ~2.5 mL, at C7-T1. A, AP view. Note essentially unilateral, vacuolated contrast pattern extending from C5 to T2. Flow of contrast into spinal nerve canals is present (broken arrows). ­Compare to Figure 35-22, A. B, Lateral view. ­Suboptimal image secondary to patient body habitus. Note wide contrast column, not confined to the dorsal epidural space, indicating spread of contrast into the lateral and ventral epidural space ­covering the proposed pathology. ­Compare to Figure 35-22, B. C, Right oblique view (i.e., contralateral to needle tip position). Note contrast clearly in the dorsal epidural space ventral to the spino-laminar line. Compare to Figure 35-22, C. D, Left oblique view (i.e., ipsilateral to needle tip). Note marked vacuolated epidural pattern (solid arrows). When the image is corrected for obliquity, the tubular ­structure, indicated by open arrows, would be situated over left uncinate line and is ­consistent with spread of contrast around the vertebral artery, indicating that the injectate is covering the ventral lateral recess, vertebral foramen, and neural ­contents. Compare to Figure 35-22, D.

Figure 35-24  AP image at lumbosacral junction. A, Superior end plate of S1 is not parallel to beam. B, Superior end plate of S1 parallel to x-ray beam (black arrow). Lateral wall of the left S1 nerve canal is identified by white arrows.

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Figure 35-25  Ipsilateral oblique view, 5 to 10 degrees, of the lumbosacral junction. A, Lateral wall of the S1 nerve canal labeled with white arrows. Dorsal foramen, DF1, and ventral foramen, VF1 of S1 outlined by black line. Dorsal, DF2, and ventral, VF2, foramen of S2 indicated by white broken lines. B, Identical unlabeled image for comparison.

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Figure 35-26  Ipsilateral oblique view, 5 to 10 degrees, of the lumbosacral junction. A, Pointer on skin indicating needle insertion point. Black circle represents needle target at the lateral rostral aspect of the S1 dorsal foramen. B, Needle is positioned within the S1 nerve canal. C, Lateral view of the lumbosacral junction. A needle is seen within the S1 nerve canal with its tip (black arrow) close to the ventral canal wall (white arrows).

verification of a safe contrast pattern with AP imaging, a lateral view  (see Fig. 35-29, G) will confirm contrast in the targeted foramen, often with spread in the ventral epidural space to the pedicle above. Lateral and AP images with and without contrast are archived to verify that the procedure has been performed as stated, with technical competence, and as a record for any medical legal questions which might arise at a future date. As noted earlier, because of anatomic variation, such as severe degenerative disc disease with intervertebral disc narrowing or marked osteophytic lesions, subpedicular access to the foramen may be limited. In this case, an infraneural approach to the foramen over the intervertebral disc might be chosen. The end plates at the specific level are squared to the x-ray beam. An ipsilateral oblique view is then obtained so that the SAP of the level below is situated under the approximate midpoint of the inferior end plate of the level above. After the skin infiltrate of local anesthetic, the procedure needle is advanced toward the intervertebral disc, just lateral to the

SAP. This technique is analogous to that used to access the intervertebral disc during discography, with advancement halted within the foramen prior to entering the disc annulus. Resistance will be noted as the annulus is contacted and a lateral view obtained to verify needle depth. (Fig. 35-30, B). The needle will be seen lying in the inferior aspect of the foramen, possibly adjacent to the intervertebral disc. An AP view is checked to ensure the needle is within the foramen in a medial-lateral orientation (see Fig. 35-30, B). When the infraneural technique is used, flow around the pedicle will not be seen in many instances. The contrast will be noted to flow through the foramen and spread within the lateral epidural space both in a rostral and caudal direction (see Fig. 35-30, C-G). When the injection of contrast produces a satisfactory pattern, the corticosteroid injectate, preferably as a solution, can be injected with confidence that safety is ensured, and the coverage of the pain generator may provide pain relief. Use of 4% lidocaine (Xylocaine) combined with the corticosteroid solution can provide

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Figure 35-27  Ipsilateral oblique view of 5 to 10 degrees. A, Plain fluorography image preinjection of contrast. B-E, Sequential digital subtraction imaging (DSI) during injection of contrast. No vascular pattern is noted flowing toward, and stopping at, the midline in the area designated by the oval.  B, DSI at start of injection, ~ 0.1 mL. C, DSI, volume of injection ~ 0.5 mL. D, DSI, volume of injection ~1.0 mL. E, DSI and end of injection ~1.75 mL. F, AP fluoroscopic image following contrast injection. Cephalad contrast flow noted to the L5-S1 disc level (arrow). G, Lateral image following contrast injection. Contrast flow noted to the L5-S1 disc level (black arrow). Note contrast flow filling the S1 nerve canal and flowing through the ventral foramen (white arrows).

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Figure 35-28  AP image at lumbosacral junction. A, Note the superior end plate of S1 is not parallel to the x-ray beam. B, Inferior end plate of L5, closest to target, is parallel to x-ray beam indicating a true AP view. C, Left oblique view. Note that the SAP of S1 appears to lie under the 6:00 o’clock position of the L5 pedicle. Circle represents needle target. D, Left oblique view. A 25-gauge, 3.5-inch Quincke pointed spinal needle is seen having been advanced into the L5-S1 foramen caudal to the 6:00 o’clock position on the pedicle. E, MRI subpedicular axial L4-5 T1 WI. Representation of needle insertion into the left midforamen. F, Lateral view of the lumbosacral junction. The tip of the 25-gauge, 3.5-inch spinal needle is seen in a subpedicular position in the midsection of the L5-S1 foramen. Broken white line indicates needle was inserted parallel to the inferior end plate of L5, showing correct initial AP positioning of the C-arm (see Fig. 35-28, B).

a final concentration that ensures sensory blockade. As noted, this can afford only negative diagnostic information, but is often a worthwhile addition. As previously noted, some practitioners have advocated the use of a “test dose” of local anesthetic prior to the corticosteroid injection. From a single reported case study,123 it is theorized that if injection into the medullary artery were to occur, local anesthetic would flow into the anterior spinal artery, thereby anesthetizing the spinal cord and producing temporary motor and sensory deficit. The corticosteroid injection would then be abandoned

and any detrimental effects of the corticosteroid injection would be prevented. This chain of suppositions depends on the assumption that a solution of corticosteroid injected into the medullary artery will cause a greater deleterious effect to the spinal cord than a solution of local anesthetic. Cord infarctions with the postulated etiology involving injection into the medullary artery, resulting in cord ischemia in the watershed of the anterior spinal artery, have been reported only with the use of particulate corticosteroid preparations. Therefore, if one limits corticosteroid use in transforaminal injections to solutions, this problem should be preventable. 

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Figure 35-29  AP digital subtraction imaging (DSI) and plain fluoroscopic images prior to, during, and postcontrast injection. A, Precontrast. The needle tip is noted as lying under the 6:00 o’clock position (black arrow) of the L5 pedicle within the “safe triangle”. The segmental nerve (broken lines) courses caudal, medial, and ventral to the needle tip. B-E, Sequential DSI during injection of contrast. Arrows indicate contrast caudal to the pedicle within the L5-S1 foramen and flowing medially into the epidural space. No vascular pattern is noted flowing toward the midline in the area designated by oval. B, DSI image at start of contrast injection, volume ~0.2 mL. C, DSI, ~0.5 mL of contrast injected. D, DSI, ~0.75 mL of contrast injected. E, DSI, at end of injection, ~1.2 mL of contrast. F, AP image after ~1.2 mL of contrast is injected. Contrast is clearly covering the course of the L5 segmental nerve and dorsal root ganglion (DRG). Arrow indicates contrast flow through the foramen into the epidural space. G, Lateral image after ~1.5 mL of contrast is injected. The white arrow notes contrast within the ventral L5-S1 foramen, while the black arrow indicates spread of contrast cephalad to the L4-5 disc level.

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Figure 35-30  Transforaminal L4-5 injection using the infraneural approach. A, AP image with needle in position in the caudal foramen. Needle tip (arrow) lies between the lateral and medial pedicular lines (white broken lines), illustrating position within the foramen. The L4 segmental nerve (black broken lines), passes rostral and ventral to the needle (see B). B, Lateral view with needle in place. Needle is noted to be in an infraneural position within the caudal foramen. Segmental nerve is outlined. C-E, AP digital subtraction imaging (DSI) sequence during injection of contrast. C, Image after injection of ~0.25 mL. Contrast (black arrow) is seen within the L4-5 foramen without spread into the epidural space. No flow is evident medial to the medial pedicular line (white broken line) and into the epidural space. D, After injection of ~1.0 mL flow is noted through the L4-5 foramen and into the epidural space. E, End of contrast injection of ~1.75 mL. Contrast is clearly seen flowing through the L4 foramen and into the epidural space. Contrast is also noted in the L5 nerve canal (arrows). F, Plain fluoroscopic image at end of contrast injection of ~1.75 mL. Contrast is clearly seen flowing through the L4-5 foramen, into the epidural space, covering the position of the L4 dorsal root ganglion (DRG) and ­segmental nerve. Contrast is also noted in the L5 nerve canal (arrows). G, Lateral view at end of ­injection. Contrast is noted within the L4-5 foramen, covering the segmental nerve and the dorsal root ganglion (DRG).

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In addition, using a test dose 2 minutes prior to injection of the corticosteroid presumes that the needle tip will not move during this period of time: a questionable supposition.

Thoracic Transforaminal Injections Fluoroscopic imaging of the thoracic spine lacks the conspicuity of the cervical and lumbar regions. The lungs, heart, great vessels, and ribs impart radiopaque shadows, and movement of the heart, chest wall, and the variability in radiolucency from the differing tissue radiolucency and air exchanges during inspiration and expiration often makes interpretation of images challenging. In addition, most practitioners have minimal experience with the thoracic spine because pain complaints in this region occur less frequently than in the lumbar and cervical areas and training specific to the thoracic spine is uncommon. Thoracic transforaminal injections are rarely indicated rostral to T4 because pathology is infrequently seen in these segments. To access the thoracic intervertebral foramina, the patient is placed prone on the procedure table. After a sterile preparation of the skin and draping, the proposed level for injection is identified. Because individual characteristics of the twelve thoracic levels are not easily identifiable (i.e., “all thoracic levels look the same”), it is of utmost importance to be compulsive about ascertaining the correct level. The authors recommend counting down from T1 and marking the skin over the pedicles of the chosen level with a marking pen ensuring that the end plate closest to the target is squared. One then counts up from T12, ensuring that this second enumeration of the specified level matches with the first (Fig. 35-31, A). If any question remains, additional examinations are performed until no doubt exists in the mind of the physician injectionist that the correct level is being targeted. A true AP view is obtained by squaring the inferior end plate of the chosen level; (i.e., T9 if the T9-10 foramen has been chosen to access (see Fig. 35-31, B). The C-arm is rotated in an ipsilateral oblique motion so that the pedicle will appear to move medially toward the midline with the rib head following. The lateral pedicular line, or SAP, is placed between one third and one half the distance over the vertebral body (Fig. 35-32, A). The foramen can be accessed anywhere between the boundary pedicles. Because the medullary artery, artery of Adamkiewicz, is found within the

rostral-ventral aspect of the foramen, usually lies caudal to T7, but can be highly variable in location, one of the authors (ML) prefers an infraneural approach, over the intervertebral disc, rather than a subpedicular, needle placement. The target is an area of hyperlucency in the form of a rectangle seen over the intervertebral disc (see Fig. 35-32, B). This so called “magic box” is bounded laterally by a line formed by connecting the medial rib heads; the lateral pedicular line/SAP; and the inferior and superior end plates of the specific level. Local anesthetic can be infiltrated and a 25- or 22-gauge spinal needle can be advanced toward the target using frequent intermittent fluoroscopy (Fig. 35-33, A). As long as the needle is directed medial to the rib head, costovertebral joint, and lateral to the lateral pedicular line, pneumothorax and central canal encroachment is nearly impossible. Often during insertion of the needle, os will be contacted. Because the needle is traversing a space between the proximal rib and SAP, rotation of the bent needle tip will permit continued advancement. Resistance will be noted as the needle contacts the annulus of the intervertebral disc, and further advancement is halted (Fig. 35-33, B and C). Acceptable needle placement in lateral and AP views is now confirmed and images are saved (see Fig. 35-33, B and Fig. 35-34, A). The needle tip as will be seen in a lateral view as lying in the caudalventral foramen, and the AP image will note its foraminal placement between the medial and lateral pedicular lines. Injection of contrast using active AP fluoroscopy, with DSI if available, will provide confirmation of flow through the foramen into the lateral epidural space without worrisome vascular uptake as detailed previously (see Fig. 35-34, B-F). The lateral view will confirm foraminal and epidural injection (Fig. 35-35). Injection of the nonparticulate corticosteroid with normal saline or local anesthetic as the diluent in a total volume of  2 to 3 mL can proceed when a safe contrast pattern that encompasses the targeted neural structure is noted.

Cervical Transforaminal As stated previously, in recent years as more physicians with differing levels of training are pursuing interventional pain procedures, a rise in the number of catastrophic outcomes from injection of particulate corticosteroids into the cervical foramen has been realized.

T7 T7 T8 T8 T9 T9 T10 T10 T11 T11

A

B

Figure 35-31  AP image of the ­thoracic spine. A, Inferior end plate of T9 and superior end plate of T10 are not parallel to beam. B, Inferior end plate of T9 and superior end plate of T10 are parallel to x-ray beam (black arrows).

Epidural Steroid Injections: Cervical, Thoracic, and Lumbar: Transforaminal, Interlaminar, and Caudal  345

35 T7 Figure 35-32  Left oblique images of the thoracic spine. The pedicles appears to have moved medially with the rib heads following. White broken line indicates medial rib heads, costovertebral joint. Black broken line delineates midpedicular line that closely approximates the lateral lamina and SAP. A, a small radiolucent so-called “magic box” is noted over the intervertebral disc, bounded by the inferior end plate of T9 (white line), the superior end plate of T10 (black line), the medial pedicular line (white broken line), and the medial rib head line (black broken line). B, Needle target over intervertebral disc (circle) is shown in this magnified image of A.

T8 T9

T9

T10 T10 T11

A

B

T9 T9

T10 T10

B

A

Lung

RH SAP

Lung

C Figure 35-33  Needle within the T9-10 foramen. A, Oblique view, needle has been advanced over the intervertebral disc between the medial rib head line and midpedicular line. B, Lateral view. Note that the needle tip (arrow) is in the infraneural position caudal and ventral within the foramen in proximity to the dorsal intervertebral disc. C, CT axial bone window image of the midthoracic spine. Note safe needle access (arrow) to the foramen between the rib head (RH) and superior articular process (SAP). As long as the needle is advanced within the “magic box”, medial to the rib head and lateral to the SAP, the lung and central spinal canal are not at risk. Black lines indicate lateral margin of the central canal.

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T9

T10

A

B

C

D

E

F

Figure 35-34  Needle is placed within the T9-10 foramen. A, AP image precontrast injection. Needle tip is in the lateral foramen (arrow) as is evident by relationship to pedicle shadow. B-E, Sequential digital subtraction imaging (DSI) series during injection of contrast. Note flow of contrast medial through foramen (black arrows). No vascular flow is evident into the midcanal (white oval), which might indicate a medullary artery injection. B, Volume ~0.25 mL. Arrow indicates flow into epidural space. C, Volume ~0.5 mL. D, Volume ~ 1.0 mL. E and F, DSI and plain fluoroscopic images at completion of contrast injection— final volume ~1.75 mL. Note the extent of spread of a relatively small volume within the foramen and epidural space. Only a small proportion of the injectate   is noted lateral along the ventral ramus (open arrows).

This is a procedure that should be shunned by those novices who have not had years of extensive experience and training in regard to the anatomy of the region and correct technique. However, the authors are not aware of any catastrophic events occurring when due diligence was practiced, all images were saved indicating safe needle placement, and a solution injectate was used. The patient is placed in supine position with a pillow under the shoulders to slightly extend the cervical region. The anterior and procedural side of the cervical region is prepared and draped sterilely. Whereas in most procedures the C-arm fluoroscope is positioned laterally, perpendicular to the patient, some experienced injectionists, including one of the authors (ML), prefer it to be positioned at the head of the procedure table for ease of obtaining views in all planes of projection. This technique lends itself to the operator sitting on the side to be targeted. The C-arm is maneuvered to obtain an oblique view with caudal tilt of the image

intensifier, so that the foramina are seen at their widest diameter in respect to both cephalocaudal and ventral-dorsal dimensions. This is the so-called “foraminal” view (Fig. 35-36). In this position, the x-ray beam is focused parallel to the exiting nerve and foramen. An essential understanding of the shape of the foramen is paramount to the safe conduct of this procedure. In this foraminal view, the actual foramen is not an aperture as it appears. In actuality, it is shaped like a funnel (Fig. 35-37) with the central part appearing hyperlucent, whereas the actual outer edge is ill defined and indistinct because it lies over the posterior and anterior boney elements. The target is the SAP of the level below, dorsal to what appears to be the sharp dorsal border of the foramen and approximately one fourth to one third cephalad of the foramen’s most caudal aspect (Fig. 35-38). The skin is marked and if desired, a skin wheal of local anesthetic can be injected. A small-gauge needle is then inserted to

Epidural Steroid Injections: Cervical, Thoracic, and Lumbar: Transforaminal, Interlaminar, and Caudal  347

contact bone, SAP, dorsal to the apparent foramen (Fig. 35-39). One of the authors (ML) prefers a slight bend on the tip of the needle to increase maneuverability and control. However, an opposing opinion (CA) prefers a straight needle because the radius circumscribed by a bent needle tip with rotation can be considered a “cutting weapon” and might damage any neural or vascular structures that are encountered. Because the actual distance between skin and foramen is rarely greater than 1.5 inches, and a slight misdirection of the needle can easily lead to placement into a potentially perilous structure (Fig. 35-40), a technique in which the needle is advanced quickly under active fluoroscopy is thought to be safest. In addition, if pressure is applied with a blunt instrument during needle insertion, soft tissue is distracted, and the actual depth to target is usually less than one-half inch. This pressure is then released and the skin draws back over the needle, securing it in place. This technique can be accomplished in less than 1 second, and some radiation exposure to the dominant hand is inevitable (see Fig. 35-39). Using

T9

T10

Figure 35-35  Lateral fluoroscopic image after injection of final contrast ­volume ~1.75 mL. Contrast is seen within the entire foramen with the targeted anatomic structure, the T9 segmental nerve, and dorsal root ganglion (DRG) clearly outlined (arrows).

C3

A

C4

C5

C6

pulsed, low-dose fluoroscopic modes, the radiation dose is low, and the perceived safety factor afforded by this technique is appealing. This  technique is analogous to that used for cervical discography and stellate ganglion blocks. When the SAP is contacted dorsal to the perceived foramen, all further advancement of the needle is immediately stopped until depth can be ascertained (Fig. 35-41, A). If the needle is additionally inserted at this point, entry into the central spinal canal can easily occur (see Fig. 35-40). An AP view (Fig. 35-41, B) verifies mediallateral position. The needle tip should be seen as lying over the midaspect of the articular pillar. The needle can be advanced toward the uncinate because the dural root sleeves in the cervical spine do not extend laterally to the degree observed in the lumbar spine and vascular structures are less prevalent in this area. At this juncture, images documenting precontrast needle position are archived. The foraminal view (Fig. 35-41, A) shows the needle in the dorsal foramen contacting the SAP, whereas the AP view (see Fig. 35-41, B) documents that encroachment of the central canal has not occurred. A needle inadvertently placed ventral within the foramen owing to slight error in angle of insertion, might easily puncture the vertebral artery. Using active fluoroscopy in the AP view, with DSI if available, contrast is injected to ensure a safe pattern. Flow should be seen through the foramen and into the lateral epidural space  (Fig. 35-42). If marked foraminal stenosis is present, minimal contrast may be seen entering the spinal canal. A transient mild to moderate, pressure paresthesia is often noted by the patient secondary to neural stimulation. If significant venous uptake is evident, the needle can be repositioned slightly, either medially toward the uncinate process or laterally, while staying in touch with the SAP. One then reinjects contrast until a safe pattern is noted. If vascular flow to the midspinal canal is evident, the medullary artery may have been cannulated, and the procedure must be terminated. If apparent filling of a tubular structure is noted lateral to the uncinate process in AP view, and over the uncinate line in foraminal view, vertebral artery injection—either intramural or intraluminal—must be considered strongly and the procedure terminated. If there is any question in the operator’s mind about the safety of the injection, the procedure should be terminated immediately. As noted above, some injectionists, including one of the authors (CA), prefer to inject a test dose of local anesthetic prior to the corticosteroid and wait 2 minutes looking for neurologic

C7

C3

C4

C5

C6

C7

B

Figure 35-36  Oblique, foraminal view of cervical spine. Foramina are at their widest extent both in dorsal-ventral and cephalocaudal diameters. A, Inner dashed circle represents the inner circumference of the most medial aspect of the foramen. The white circle represents the true margin of the foramen. The needle target is indicated by a black dot. B, Identical image for comparison.

35

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C6

C7

Figure 35-39  Oblique, foraminal view of cervical spine. Foramina are at their widest extent both in dorsal-ventral and cephalocaudal diameters. Indicating the target and with pressure providing distraction of soft tissues and decreasing the skin-target distance, the needle is advanced quickly, and the C7 superior articular process (SAP) is contacted dorsal to the apparent foramen.

Figure 35-37  MRI axial T2 WI. Shape of cervical foramen seen as “funnel”. Note medial diameter is smaller than lateral diameter.

C6

C7

Figure 35-38  Oblique, foraminal view of cervical spine. Target foramen is seen at its widest extent both in dorsal-ventral and cephalocaudal diameters. Black dashed circle represents the inner circumference of the most medial aspect of the foramen. The white circle represents the true margin of the foramen. The two broken lines represent the approximate position of the vertebral artery overlying the uncinate line. The pointer indicates the needle target over the midportion of the C7 SAP dorsal to the foramen.

sequelae correlated with an anesthetized spinal cord. When a safe contrast pattern has been obtained in both AP and foraminal views (see Figs. 35-42, E and 35-43), images are saved for the historical record of the procedure. The nonparticulate corticosteroid can be injected with diluent of choice.

Figure 35-40  MRI axial T2 WI. Solid arrow indicates correct needle trajectory contacting the superior articular process dorsal to the foramen. The broken arrow indicates targeting of what appears to be the dorsal aspect of the radiolucent foramen when seen in an oblique, foraminal view. A very small miscalculation in the angle of insertion can result in marked morbidity as the vertebral artery or spinal canal is entered. Note left lateral extrusion (black arrow).

Postprocedure Care Following the injection, whether cervical, thoracic, or lumbar, the needle is removed and the skin is cleansed of the antiseptic solution and any blood. A sterile self-adhesive dressing can be applied if desired. The patient is taken to a recovery area for observation where physiologic monitoring is continued until discharge. Recovery room personnel should be trained to recognize any emergent situations

Epidural Steroid Injections: Cervical, Thoracic, and Lumbar: Transforaminal, Interlaminar, and Caudal  349

35

A

B

Figure 35-41  A, Oblique, foraminal view of cervical spine. The needle in position contacting the C7 superior articular process (SAP) dorsal to the apparent foramen. Needle is dorsal to the vertebral artery (broken white lines). B, AP view of cervical spine. The needle tip (white arrow) in position contacting the SAP over the midsection of the articular pillar (black double-headed arrow). Note distance from uncinate line that indicates the most lateral extent of dural root sleeve position and possible spinal canal trespass. The vertebral artery (white dashed lines) is ventral to the needle position in the dorsal foramen.

A

B

C

DRG

D

DRG

E

Figure 35-42  Sequential AP views of the cervical spine during injection of contrast. No vascular injection is evident either flowing towards, at the midline which might indicate an injection into the medulary artery with flow into the anterior spinal artery. See area bounded by the oval. No tubular contrast enhanced structure is noted coursing in a cephalocaudal orientation lateral to the uncinate line indicating vertebral artery injection. A, At start of contrast injection, approximate volume is 0.2 mL. Note extent of foramen clearly is identified (black arrows). If one wished to perform a so-called “selective spinal nerve block” (SSNB), a volume ≤0.3 mL of concentrated local anesthetic might provide selectivity. B, Injection at an approximate volume of 0.75 mL. At this point, contrast is seen entering the spinal canal. Lateral flow along ventral ramus is seen (arrow). C, Injection at an approximate volume of 1.25 mL. At this point, contrast is seen entering the spinal canal (white arrow). Increasing lateral flow along ventral ramus is evident (black arrow). D, Injection at an approximate volume of 1.75 mL. At this point, contrast is clearly noted within the spinal canal (white arrows). The dorsal root ganglion (DRG) is identified within the foramen. Increased lateral flow along ventral ramus continues (black arrow). E, AP view of cervical spine contrast volume of ~1.75 mL. At this point, contrast is clearly noted within the spinal canal (white arrows). The DRG is identified within the foramen. Increased lateral flow along ventral ramus continues (black arrow).

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reasonably expected. If sensory deficit in the selected target dermatome was noted, but the patient continued to realize his initial level of pain, either a technical problem occurred or the diagnosis of L5 radicular pain must be reconsidered. This postprocedure evaluation must be included in the specific, detailed, accurate procedure note dictated following any medical intervention (see appendix A and B). On discharge, written instructions should be provided to the patient. These instructions should detail information about a follow-up appointment, care of the injected area, and on contacting medical help if the patient experiences a complication due to the procedure.

Summary

Figure 35-43  Oblique, foraminal view of cervical spine. Contrast is noted within the dorsal foramen and epidural space. No contrast is noted filling a tubular structure over the uncinate [i.e., the vertebral artery (parallel white brokenlines]. Foraminal contrast over articular pillar is evident (arrows).

that may present. Complications require diagnosis and treatment in a timely and appropriate manner. Although rarely needed, immediate access to oxygen, airway supplies, and emergency medications must be available. Because sensory and/or motor deficit is often noted when local anesthetics are used, neurologic assessment is of particular importance. If a lumbar injection has been completed, it is prudent to ascertain that the patient has sufficient control of the lower extremities to stand and walk, and assistance on rising should be initially provided. Any motor deficit will rapidly reverse if reasonable doses of local anesthetic were used. Prior to discharge, if a more selective injection (i.e., transforaminal versus interlaminar) was completed with local anesthetic, the patient is evaluated for degree of pain relief compared with initial, preprocedure level. Assessment by the physician, or other trained personnel, must include those provocative movements which initiate an increase in the index pain. Appraisal of pain intensity change following a procedure with the patient lying comfortably in a bed is of no value. Following an L5-S1 transforaminal injection, the postprocedure neurologic examination would be expected to evidence weakness in extensor hallucis longus, and sensory decrease of the dorsal foot and great toe. These findings validate the procedure because if present, a response to the corticosteroid might be

Corticosteroids placed within the epidural space are rationally used for treatment of radicular type pain thought to originate from inflammation whether lumbar, thoracic, or cervical. Common sense dictates that an injection specifically and precisely targeting the pain generator with a concentrated active component will have more benefit when compared to a dilute preparation placed in an area distanced from the pathology. This is borne out in the literature where precise, selective, transforaminal epidural placement of corticosteroids have shown long-term benefit. Conversely, nonfluoroscopically guided “epidurals,” more precisely designated “injections of corticosteroid placed somewhere in or near the spine,” have been shown to have no clinically significant efficacy. Blind, nonfluoroscopically validated “epidural” injections, can no longer be considered to meet a contemporary standard of medical care, and ethics dictate that this practice be relegated to historical interest only. In addition, the questionable practice of “a series of three epidurals” must be abandoned as having no scientific rationale. Evaluation of the patient following each injection and basing further treatment on some evidence of past benefit and a rational expectation of future pain relief is the essence of evidence-guided medicine. Today, for the vast majority of patients with radicular pain, prior to any surgical intervention, transforaminal injection of corticosteroid must be considered the treatment of choice. That these routine procedures are “special,” “dangerous,” or noneffective speaks to the questionable training of those espousing these sentiments. As with all medical interventions, there is a risk-benefit ratio that must be considered. Transforaminal and interlaminar ­epidural injections can involve significant morbidity and even mortality. However, with prudence, vigilance, and meticulous technique, these risks are well managed by a fully trained Interventional Pain Management/Nonsurgical Spine Specialist.

Sample Dictation for Lumbar Interlaminar Epidural Injectionist: Dr. Needle History: See dictated consultation of 5 May. Ms. Jones suffers from low back pain with radiation into the lower extremities bilaterally R > L with walking. The pain is relieved with sitting. MRI evidences moderate-to-severe spinal stenosis of 6.5 mm at L3-4. Patient has undergone epidural injections with corticosteroid in the past with months of good relief. Preop/Postop diagnosis Lumbar radicular pain ll Lumbar spinal stenosis ll Procedures ll Lumbar epidural injection via interlaminar approach ll Fluoroscopy for needle guidance ll Procedure ll

ll

Informed consent was obtained from the patient regarding risks and complications. Postdural puncture headache was discussed. Mrs. Jones elected to proceed after all questions were answered. She was taken to a procedure room where she was placed in prone position. The lumbosacral region was prepped and draped in a sterile manner. A fluoroscope was used to examine the lumbar spine. Five lumbar non–rib-bearing vertebral bodies were noted. Degenerative changes including degenerative disc disease,

A

“Z” joint hypertrophy, and osteophytic lesions were noted. The L4-5 interlaminar space was identified. A skin wheal was made with local anesthetic and carried down to 1.5 inches. An 18 gauge Hustead needle was advanced toward the right interlaminar space. Ligamentum flavum was contacted. Loss of resistance to saline and air identified the epidural space. No CSF or blood was noted with aspiration. Isovue 200, 3 mL was injected and an epidural pattern noted, right greater than left, with contrast clearly identified within the right L4 and L5 foramen. There was decrease contrast flow evidenced rostral to the L3-4 disc level. A lateral view confirmed epidural contrast without intrathecal injection. This was followed by injection of methylprednisolone 80 mg in normal saline 2 mL, total volume 3 mL. During injection the patient noted “pressure” into the right hip, buttock, and thigh, which was noted to be concordant to the index pain. Mrs. Jones tolerated the procedure well and was taken to recovery in stable condition. Mrs. Jones was discharged home in her husband’s care and will follow up with her PCP, Dr. Smith in the near future. She will follow up with this physician if any problems occur or in 2 weeks by telephone because she lives 4 hours from this facility. She understands that if two to three epidural corticosteroid injections in any 6-month period provide good relief and allow her to maintain her activities of daily living, this is an appropriate palliative treatment modality.

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Sample Dictation for Cervical Transforaminal Injectionist: Dr. Needle History: See dictated consultation. Mr. Jones suffers from neck pain radiating into the left upper extremity into digits 1 and 2. MRI shows a large extrusion on the left at C5-6. Preop diagnosis Cervical radicular pain ll Extrusion L C5-6 ll Postop diagnosis ll Same ll Procedures ll Transforaminal injection C5-6 left ll Fluoroscopy for needle guidance ll Procedure ll

ll

Informed consent was obtained from the patient regarding risks and complications including quadriplegia and death. All questions were answered and possible alternatives were discussed. Mr. Jones elected to proceed. Mr. Jones was taken to a procedure room where he was placed in supine position with a pillow under the shoulders to slightly extend the neck. The head was slightly rotated to the right. The anterior and left cervical regions were prepped and draped in a sterile manner. A fluoroscope was used to examine the cervical spine. Using a left “foraminal view” the C5-6 foramen was identified by counting down from the C2-3 foramen three times. The foramen diameters in ventral-dorsal and rostral-caudal were maximized.  A skin wheal with local anesthetic was made, and while applying

B

pressure with a blunt instrument, a 25 gauge, 3.5-inch spinal needle was advanced. Os was contacted on the superior articular process of C6 dorsal to the foramen. The pressure with the blunt instrument was withdrawn. An AP view showed the needle tip lying over the midsection of the articular pillar. Using a 3 mL syringe with a small-bore, low-volume extension tubing, iopamidol 200, 0.5 mL was injected using DSI. Significant venous uptake was noted. Staying in contact with bone, the needle was advanced slightly toward the uncinate process. Once again with DSI, Isovue 200, 1.25 mL was injected and flow was noted medially through the foramen into the epidural space. No vascular uptake was appreciated. The DRG was clearly identified. A foraminal view noted contrast in the dorsal foramen. Injection was then made using a solution of dexamethasone 10 mg with lidocaine (Xylocaine) 4% MPF 0.5 mL, total volume 1.5 mL. Transient mild pressure paresthesia into the upper extremity was noted by the patient, which was concordant with his usual pain complaint. Mr. Jones tolerated the procedure well and was taken to recovery in stable condition. Thirty minutes postprocedure, he evidenced a marked C6 sensory deficit owing to the local anesthetic effect, and noted “95%” relief of his usual, preprocedure pain with provocative movements. Although not diagnostic, this indicates probable coverage of the pain generator. He was discharged home in stable condition in his wife’s care. He will follow up in 2 to 3 weeks for reevaluation and possible additional injections, if appropriate.

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REFERENCES  1. Evans W. Intrasacral epidural injection in the treatment of sciatica. Lancet. 1930;2:1225.  2. Robecchi A, Capra R. Intrasacral epidural injection in the treatment of sciatica. Minerva Med. 1952;98:1259.  3. Lievre JA, Bloch-Michel H, Pean G. L’hydrocortisone en injection locale. Rheumatism. 1953;20:310.  4. Gardner WJ, Goebert Jr HW, Sehgal AD. Intraspinal corticosteroids in the treatment of sciatica. Trans Am Neurol Assoc. 1961;86:214-215.  5. Barry PJ, Kendall PH. Corticosteroid infiltration of the extradural space. Ann Phys Med. 1962;6:267-273.  6. Goebert Jr HW, Jallo SJ, Gardner WJ, et al. Painful radiculopathy treated with epidural injections of procaine and hydrocortisone acetate: Results in 113 patients. Anesth Analg. 1961;40:130-134.  7. Krempen JF, Smith BS. Nerve-root injection: A method for evaluating the etiology of sciatica. J Bone Joint Surg Am. 1974;56:1435-1444.  8. Tajima T, Furukawa K, Kuramochi E. Selective lumbosacral radiculography and block. Spine. 1980;5:68-77.  9. Stanley D, McLaren MI, Euinton HA, et al. A prospective study of nerve root infiltration in the diagnosis of sciatica. A comparison with radiculography, computed tomography, and operative findings. Spine. 1990;15:540-543.   10. Catchlove RF, Braha R. The use of cervical epidural nerve blocks in the management of chronic head and neck pain. Can Anaesth Soc J. 1984;31:188-191.   11. Rowlingson JC, Kirschenbaum LP. Epidural analgesic techniques in the management of cervical pain. Anesth Analg. 1986;65:938-942.   12. Warfield CA, Biber MP, Crew DA, et al. Epidural steroid injection in the treatment for cervical radiculitis. Clin J Pain. 1988;4:201-204.   13. Morvan G, Mempoint D, Bard M, et al. Direct intra-foraminal injection of corticosteroids in the treatment of cervico-brachial pain. In: Baird M, Laredo J, eds. Interventional Radiology in Bone and Joint. New York: Springer Verlag; 1988:25.   14. Bush K, Hillier S. Outcome of cervical radiculopathy treated with periradicular/epidural corticosteroid injections: A prospective study with independent clinical review. Eur Spine J. 1996;5:319-325.   15. Vallee JN, Feydy A, Carlier RY, et al. Chronic cervical radiculopathy: Lateral-approach periradicular corticosteroid injection. Radiology. 2001;218:886-892.   16. Slipman CW, Lipetz JS, Jackson HB, et al. Therapeutic selective nerve root block in the nonsurgical treatment of atraumatic cervical spondylotic radicular pain: A retrospective analysis with independent clinical review. Arch Phys Med Rehabil. 2000;81:741-746.   17. Forrest JB. Management of chronic dorsal root pain with epidural steroid. Can Anaesth Soc J. 1978;25:218-225.   18. Ramamurthy S. Thoracic epidural block. In: Waldman SD, ed. Interventional Pain Medicine. 2nd ed. Philadelphia: WB Saunders; 2001:390.   19. Yin W. A posterior parasagittal approach to thoracic paravertebral structures with curved cannulae. Tech Regl Anesth Pain Manag. 2001;5:157.   20. Friedly J, Chan L, Deyo R. Increases in lumbosacral injections in the Medicare population: 1994 to 2001. Spine. 2007;32:1754-1760.   21. Carrino JA, Morrison WB, Parker L, et al. Spinal injection procedures: Volume, provider distribution, and reimbursement in the U.S. medicare population from 1993 to 1999. Radiology. 2002;225:723-729.   22. Vroomen PC, de Krom MC, Slofstra PD, Knottnerus JA. Conservative treatment of sciatica: A systematic review. J Spinal Disord. 2000;13:463-469.   23. Levin JH. Prospective, double-blind, randomized placebo-controlled trials in interventional spine: What the highest quality literature tells us. Spine J. 2009;9:690-703.   24. Fitzgibbon DR, Posner KL, Domino KB, et al. Chronic pain management: American Society of Anesthesiologists Closed Claims Project. Anesthesiology. 2004;100:98-105.   25. Wiltse LL, Fonseca AS, Amster J, et al. Relationship of the dura, Hofmann’s ligaments, Batson’s plexus, and a fibrovascular membrane lying on the posterior surface of the vertebral bodies and attaching to the deep layer of the posterior longitudinal ligament. An anatomical, radiologic, and clinical study. Spine. 1993;18:1030-1043.

  26. Tarlov IM. Spinal perineurial and meningeal cysts. J Neurol Neurosurg Psychiatry. 1970;33:833-843.   27. Langdown AJ, Grundy JR, Birch NC. The clinical relevance of Tarlov cysts. J Spinal Disord Tech. 2005;18:29-33.   28. Beaujeux R, Wolfram-Gabel R, Kehrli P, et al. Posterior lumbar epidural fat as a functional structure? Histologic specificities. Spine. 1997;22:1264-1268.   29. Scapinelli R. Anatomical and radiologic studies on the lumbosacral meningo-vertebral ligaments of humans. J Spinal Disord. 1990;3:6-15.   30. Blomberg R. The dorsomedian connective tissue band in the lumbar epidural space of humans: An anatomical study using epiduroscopy in autopsy cases. Anesth Analg. 1986;65:747-752.   31. Crock HV, Yoshizawa H, Kame SK. Observations on the venous drainage of the human vertebral body. J Bone Joint Surg Br. 1973;55:528-533.   32. Gershater R, St Louis EL. Lumbar epidural venography. Review of 1,200 cases. Radiology. 1979;131:409-421.   33. Dommisse GT. The Arteries and Veins of the Human Spinal Cord from Birth. New York: Churchill Livingstone; 1975:51.   34. Turnbull IM, Brieg A, Hassler O. Blood supply of cervical ­spinal cord in man. A microangiographic cadaver study. J Neurosurg. 1966; 24:951-965.   35. Launay M, Chiras J, Bories J. Angiography of the spinal cord: Venous phase. Normal features. Pathological application. J Neuroradiol. 1979; 6:287-315.   36. Dommisse GF. The arteries, arterioles, and capillaries of the spinal cord. Surgical guidelines in the prevention of postoperative paraplegia. Ann R Col Surg Engl. 1980;62:369-376.   37. Huntoon MA. Anatomy of the cervical intervertebral foramina: Vulnerable arteries and ischemic neurologic injuries after transforaminal epidural injections. Pain. 2005;117:104-111.   38. Doppman J, Di Chiro G. The arteria radicularis magna: Radiographic anatomy in the adult. Br J Radiol. 1968;41:40-45.   39. Lo D, Vallee JN, Spelle L, et al. Unusual origin of the artery of Adamkiewicz from the fourth lumbar artery. Neuroradiology. 2002;44:153-157.   40. Parke WW, Watanabe R. The intrinsic vasculature of the lumbosacral spinal nerve roots. Spine. 1985;10:508-515.   41. Lazorthes G, Poulhes J, Bastide G, et al. [Arterial vascularization of the spine; anatomic research and applications in pathology of the spinal cord and aorta]. Neurochirurgie. 1958;4:3-19.   42. Merskey H, Bogduk N, Eds. Classification of Chronic Pain. Descriptions of Chronic Pain Syndromes and Definition of Pain Terms. 2nd ed. Seattle: IASP Press; 1994.   43. Smyth MJ, Wright V. Sciatica and the intervertebral disc. An experimental study. J Bone Joint Surg Am. 1958;40A:1401-1418.   44. Govind J. Lumbar radicular pain. Aust Fam Physician. 2004;33:409-412.   45. Okada E, Matsumoto M, Ichihara D, et al. Aging of the cervical spine in healthy volunteers: A 10-year longitudinal magnetic resonance imaging study. Spine. 2009;34:706-712.   46. Ernst CW, Stadnik TW, Peeters E, et al. Prevalence of annular tears and disc herniations on MR images of the cervical spine in symptom free volunteers. Eur J Radiol. 2005;55:409-414.   47. Boos N, Rieder R, Schade V, et al. 1995 Volvo Award in clinical sciences. The diagnostic accuracy of magnetic resonance imaging, work perception, and psychosocial factors in identifying symptomatic disc herniations. Spine. 1995;20:2613-2625.   48. Tafazal S, Ng L, Chaudhary N, et al. Corticosteroids in peri-radicular infiltration for radicular pain: A randomised double blind controlled trial. One year results and subgroup analysis. Eur Spine J. 2009;18:1220-1225.   49. Schofferman J, Anderson D, Hines R, et al. Childhood ­psychological trauma and chronic refractory low-back pain. Clin J Pain. 1993; 9:260-265.   50. Nickel R, Egle UT, Hardt J. Are childhood adversities relevant in patients with chronic low back pain? Eur J Pain. 2002;6:221-228.   51. Linton SJ. A prospective study of the effects of sexual or physical abuse on back pain. Pain. 2002;96:347-351.   52. Wang CL, Cohan RH, Ellis JH, et al. Frequency, outcome, and appropriateness of treatment of nonionic iodinated contrast media reactions. AJR Am J Roentgenol. 2008;191:409-415.

Epidural Steroid Injections: Cervical, Thoracic, and Lumbar: Transforaminal, Interlaminar, and Caudal  355   53. Shetty SK, Nelson EN, Lawrimore TM, Palmer WE. Use of gadolinium chelate to confirm epidural needle placement in patients with an iodinated contrast reaction. Skeletal Radiol. 2007;36:301-307.   54. Solomon R, Dumouchel W. Contrast media and nephropathy: Findings from systematic analysis and Food and Drug Administration reports of adverse effects. Invest Radiol. 2006;41:651-660.   55. Parra D, Legreid AM, Beckey NP, et al. Metformin monitoring and change in serum creatinine levels in patients undergoing radiologic procedures involving administration of intravenous contrast media. Pharmacotherapy. 2004;24:987-993.   56. Hodgson PS, Neal JM, Pollock JE, Liu SS. The neurotoxicity of drugs given intrathecally (spinal). Anesth Analg. 1999;88:797-809.   57. Braid DP, Scott DB. The systemic absorption of local analgesic drugs. Br J Anaesth. 1965;37:394-404.   58. Covino B. Clinical pharmacology of local anesthetic agents. In: Cousins M, Bridenbaugh P, eds. Neural Blockade in Clinical Anesthesia and Management of Pain. Philadelphia: JB Lippincott; 1988:111.   59. Jorfeldt L, Lofstrom B, Pernow B, et al. The effect of local anaesthetics on the central circulation and respiration in man and dog. Acta Anaesthesiol Scand. 1968;12:153-169.   60. Mather LE, Tucker GT, Murphy TM, et al. Cardiovascular and subjective central nervous system effects of long-acting local anaesthetics in man. Anaesth Intensive Care. 1979;7:215-221.   61. Benyamin RM, Vallejo R, Kramer J, Rafeyan R. Corticosteroid induced psychosis in the pain management setting. Pain Physician. 2008; 11:917-920.   62. Tuel SM, Meythaler JM, Cross LL. Cushing’s syndrome from epidural methylprednisolone. Pain. 1990;40:81-84.   63. Benzon HT. Epidural steroid injections for low back pain and lumbosacral radiculopathy. Pain. 1986;24:277-295.   64. Gaul C, Neundorfer B, Winterholler M. Iatrogenic (para-) spinal abscesses and meningitis following injection therapy for low back pain. Pain. 2005;116:407-410.   65. Kaspar J, Kaspar S, Orme C, et al. Intra-articular steroid hip injection for osteoarthritis: A survey of orthopedic surgeons in Ontario. Can J Surg. 2005;48:461-469.   66. Ward A, Watson J, Wood P, et al. Glucocorticoid epidural for sciatica: Metabolic and endocrine sequelae. Rheumatology (Oxford). 2002; 41:68-71.   67. Gonzalez P, Laker SR, Sullivan W, et al. The effects of epidural betamethasone on blood glucose in patients with diabetes mellitus. PM R. 2009;1:340-345.   68. Younes M, Neffati F, Touzi M, et al. Systemic effects of epidural and intra-articular glucocorticoid injections in diabetic and non-diabetic patients. Joint Bone Spine. 2007;74:472-476.   69. Manchikanti L, Pampati V, Beyer C, et al. The effect of neuraxial steroids on weight and bone mass density: A prospective evaluation. Pain Physician. 2000;3:357-366.   70. Bernat JL. Intraspinal steroid therapy. Neurology. 1981;31:168-171.   71. Windsor RE, Storm S, Sugar R. Prevention and management of complications resulting from common spinal injections. Pain Physician. 2003;6:473-483.   72. Kabbara A, Rosenberg SK, Untal C. Methicillin-resistant Staphylococcus aureus epidural abscess after transforaminal epidural steroid injection. Pain Physician. 2004;7:269-272.   73. Hooten WM, Kinney MO, Huntoon MA. Epidural abscess and meningitis after epidural corticosteroid injection. Mayo Clin Proc. 2004;79:682-686.   74. Furman MB, O’Brien EM, Zgleszewski TM. Incidence of intravascular penetration in transforaminal lumbosacral epidural steroid injections. Spine. 2000;25:2628-2632.   75. Furman MB, Giovanniello MT, O’Brien EM. Incidence of intravascular penetration in transforaminal cervical epidural steroid injections.  Spine. 2003;28:21-25.   76. Kim do W, Han KR, Kim C, Chae YJ. Intravascular flow patterns in transforaminal epidural injections: A comparative study of the cervical and lumbar vertebral segments. Anesth Analg. 2009;109:233-239.

  77. Botwin KP, Castellanos R, Rao S, et al. Complications of fluoroscopically guided interlaminar cervical epidural injections. Arch Phys Med Rehabil. 2003;84:627-633.   78. Cicala RS, Thoni K, Angel JJ. Long-term results of cervical epidural steroid injections. Clin J Pain. 1989;5:143-145.   79. Botwin KP, Baskin M, Rao S. Adverse effects of fluoroscopically guided interlaminar thoracic epidural steroid injections. Am J Phys Med Rehabil. 2006;85:14-23.   80. Horlocker TT, Wedel DJ, Benzon H, et al. Regional anesthesia in the anticoagulated patient: Defining the risks (the second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med. 2003;28:172-197.   81. Stoll A, Sanchez M. Epidural hematoma after epidural block: Implications for its use in pain management. Surg Neurol. 2002;57: 235-240.   82. Williams KN, Jackowski A, Evans PJ. Epidural haematoma requiring surgical decompression following repeated cervical epidural steroid injections for chronic pain. Pain. 1990;42:197-199.   83. Layton KF, Kallmes DF, Horlocker TT. Recommendations for anticoagulated patients undergoing image-guided spinal procedures. AJNR Am J Neuroradiol. 2006;27:468-470.   84. Schulman J. Treatment of neck pain with cervical epidural steroid injection. Reg Anesth. 1986;11:92-94.   85. Derby R, Lee SH, Kim BJ, et al. Complications following cervical epidural steroid injections by expert interventionalists in 2003. Pain Physician. 2004;7:445-449.   86. Hodges SD, Castleberg RL, Miller T, et al. Cervical epidural steroid injection with intrinsic spinal cord damage. Two case reports. Spine. 1998;23:2137-2142.   87. Tripathi M, Nath SS, Gupta RK. Paraplegia after intracord injection during attempted epidural steroid injection in an awake-patient. Anesth Analg. 2005;101:1209-1211.   88. Pounder D, Elliott S. An awake patient may not detect spinal cord puncture. Anaesthesia. 2000;55:194.   89. Mayall MF, Calder I. Spinal cord injury following an attempted thoracic epidural. Anaesthesia. 1999;54:990-994.   90. Baker R, Dreyfuss P, Mercer S, Bogduk N. Cervical transforaminal injection of corticosteroids into a radicular artery: A possible mechanism for spinal cord injury. Pain. 2003;103:211-215.   91. Rathmell JP, Aprill C, Bogduk N. Cervical transforaminal injection of steroids. Anesthesiology. 2004;100:1595-1600.   92. Bogduk N, Dreyfuss P, Baker R, et al. Complications of spinal diagnostic and treatment procedures. Pain Med. 2008;9:S11-S34.   93. Brouwers PJ, Kottink EJ, Simon MA, Prevo RL. A cervical anterior spinal artery syndrome after diagnostic blockade of the right C6-nerve root. Pain. 2001;91:397-399.   94. Houten JK, Errico TJ. Paraplegia after lumbosacral nerve root block: Report of three cases. Spine J. 2002;2:70-75.   95. Glaser SE, Falco F. Paraplegia following a thoracolumbar transforaminal epidural steroid injection. Pain Physician. 2005;8:309-314.   96. Yin W, Bogduk N. Retrograde filling of a thoracic spinal artery during transforaminal injection. Pain Med. 2009;10:689-692.   97. Scanlon GC, Moeller-Bertram T, Romanowsky SM, Wallace MS. ­Cervical transforaminal epidural steroid injections: More dangerous than we think? Spine. 2007;32:1249-1256.   98. Kennedy DJ, Dreyfuss P, Aprill CN, Bogduk N. Paraplegia following image-guided transforaminal lumbar spine epidural steroid injection: Two case reports. Pain Med. 2009;10:1389-1394.   99. Karasek M, Bogduk N. Temporary neurologic deficit after cervical transforaminal injection of local anesthetic. Pain Med. 2004;5: 202-205. 100. Derby R, Lee SH, Date ES, et al. Size and aggregation of corticosteroids used for epidural injections. Pain Med. 2008;9:227-234. 101. Tiso RL, Cutler T, Catania JA, Whalen K. Adverse central nervous system sequelae after selective transforaminal block: The role of corticosteroids. Spine J. 2004;4:468-474.

B

356  Spine 102. Dreyfuss P, Baker R, Bogduk N. Comparative effectiveness of cervical transforaminal injections with particulate and nonparticulate corticosteroid preparations for cervical radicular pain. Pain Med. 2006;7:237-242. 103. Okubadejo GO, Talcott MR, Schmidt RE, et al. Perils of intravascular methylprednisolone injection into the vertebral artery. An animal study. J Bone Joint Surg Am. 2008;90:1932-1938. 104. Dawley JD, Moeller-Bertram T, Wallace MS, Patel PM. Intra-arterial injection in the rat brain: Evaluation of steroids used for transforaminal epidurals. Spine. 2009;34:1638-1643. 105. Renfrew DL, Moore TE, Kathol MH, et al. Correct placement of epidural steroid injections: Fluoroscopic guidance and contrast administration. AJNR Am J Neuroradiol. 1991;12:1003-1007. 106. White AH, Derby R, Wynne G. Epidural injections for the treatment of low back pain. Spine. 1980;5:78-86. 107. Stitz MY, Sommer H. Accuracy of blind versus fluoroscopically guided caudal epidural injections. Spine. 1999;24:1371-1376. 108. Judge Janice Clark. State of Louisiana 19th Judicial District, #536,009, Spinal Diagnostics Center of Baton Rouge versus Louisiana State Board of Nursing, 10 January 2007. 109. American Medical Association House of Delegates. Resolution #903. Interventional Pain Management: Advancing Advocacy to Protect Patients from Treatment by Unqualified Providers: 24 September 2007. 110. International Spine Intervention Society. Position Statement. Prerequisite Training for the Performance of Spine Interventions. 25 September 2006. 111. American Society of Anesthesiologists. Committee on Pain Medicine. Statement on Nurse Anesthesia Training in Pain Medicine. 25 March 2004. 112. Fenton DS, Czervionke LF. Selective Nerve Root Block. In: Fenton DS, Czervionke LF, eds. Image-Guided Spine Intervention. Philadelphia: Saunders; 2003:73-97.

113. Bogduk N, ed. Practice Guidelines: Spinal Diagnostic & Treatment Procedures. San Francisco: International Spine Intervention Society; 2004. 114. Pauza KJ. PASSOR Educational Guidelines for the performance of spinal injection procedures. PASSOR Board of Governors and AAPMR Board of Governors; 2001. 115. Bogduk N. Sharp vs. blunt needles—International Spine Intervention Society White Paper. Interventional Spine. 2006;5:7-13. 116. Pauza K. A comparison of blunt vs. sharp needles with respect to intravascular injection. International Spine Intervention Society, Annual Meeting, Salt Lake City; 2006. 117. Derby R, Date ES, Lee CH, et al. Size and aggregation of corticosteroids used for epidural injections. Interventl Spine. 2006;5:30-37. 118. Bogduk N, ed. Practice Guidelines: Spinal Diagnostic & Treatment Procedures. San Francisco: International Spine Intervention Society; 2004. 119. Derby R. Point of view: cervical epidural steroid injection with intrinsic spinal cord damage: two case reports. Spine. 1998;23:2141-2142. 120. Aldrete JA, Mushin AU, Zapata JC, Ghaly R. Skin to cervical epidural space distances as read from magnetic resonance imaging films: Consideration of “hump pad”. J Clin Anesth. 1998;10:309-313. 121. Alleyne Jr CH, Cawley CM, Shengelaia GG, Barrow DL. Microsurgical anatomy of artery of Adamkiewicz and its segmental artery.  J Neurosurg. 1998;89:791-795. 122. Bogduk N, ed. Lumbar transforaminal injection of corticosteroids. In Practice Guidelines: Spinal Diagnostic & Treatment Procedures. San Francisco: International Spine Intervention Society; 2004:163-187. 123. Karasek M, Bogduk N. Temporary neurological deficit after cervical transforaminal injection of local anesthetic. Pain Med. 2004;5:202-205.

Zygapophysial Joint Pain: ­Procedures for Diagnosis and Treatment

36

Wade King, MB, BS, MMedSc, MMed(Pain), DMM, FAFMM, and James MackIntosh Borowczyk, BSc, MB, ChB, MMed(Pain), DMM, FRCP(Edin), FAFMM Zygapophysial joint (ZJ) pain stems from synovial ZJs, which are formed by adjacent articular processes (or apophyses) of the vertebrae. In the past, these joints were commonly called “facet joints” but that term is inappropriate because most synovial joints of the body (such as those of the elbows, wrists, and hands) have facets. The term “zygapophysial joints” is the correct name for the spinal synovial joints in current anatomic nomenclature.1 The phenomenon of lumbar ZJ pain was first mooted in 19112 and gradually gained acceptance,3,4 but since the 1930s when intervertebral disc surgery became feasible as a treatment for spinal pain, ZJ pain has been overshadowed in the minds of many by disc pain. Cervical ZJ pain has been established scientifically for only the last few decades.5,6 Over that time, a great deal of scientific research has been done and a considerable body of literature has been produced. ZJ pain has also generated considerable interest in clinical, funding, and medicolegal fields. Controversies have arisen about the etiology of ZJ pain and about the reliability, validity, and effectiveness of methods used to address it. Against that background, it is important for clinicians to appreciate the methods available for the diagnosis and treatment of ZJ pain and the scientific evidence on which they are based.

Zygapophysial Joints Anatomy The ZJs are paired synovial joints that link the posterior elements of the spine from the C2-3 level down to the lowest spinal motion segment, L5-S1.7 At each of these cervical, thoracic, and lumbar spinal levels, the two adjacent vertebrae are linked by three articulations: at the front is a synarthrodial interbody joint linking the anterior spinal elements (the vertebral bodies) and at the back are two diarthrodial (synovial) ZJs, one on the left and one on the right, linking the posterior spinal elements (the neural arches of the vertebrae that enclose the spinal canal8) as indicated in Figure 36-1. A ZJ is made up of two bony processes or apophyses, a superior and an inferior articular process, each of which has an articular surface (or facet) lined with hyaline cartilage about 1 to 2 mm. thick.9 Under the cartilage is a thickened layer of the subchondral bone. The joint surfaces are enveloped by a collagenous articular capsule which has superior and inferior capsular recesses above and below the main joint space.10,11 The joint space, including the recesses, is

typically of about 1 mL in volume.12 The capsule is lined internally with synovial membrane, which with the cartilaginous joint surfaces, encloses the joint space. Within the joint space but outside the synovial membrane there are often intraarticular inclusions, the most common being adipose tissue pads and fibroadipose meniscoids.13 The morphologic features of specific cervical, thoracic and lumbar joints will be addressed in the following section on bio­mechanics and the sections on the various interventional procedures. The nerve supply of the ZJs is via the medial branches of the dorsal rami of the spinal nerves.5,14,15 More specifically, the ZJs are supplied by articular branches of the medial branches; these articular branches are simply groups of medial branch dendrites that join the main trunks of their respective medial branches in the posterior parts of their courses. The joint capsules are richly innervated by sensory afferent fibers (first order neurons) which transmit neural impulses from each joint via the medial branch nerves to their cell bodies in the dorsal root ganglia and then on to synapse with second order neurons in the dorsal horn of the spinal cord; from there impulses are transmitted via central pathways to the sensory cortex. Most ZJs are supplied by two medial branches, those of the spinal nerves above and below the joint. In the cervical spine from C3-4 down the two medial branches that supply each joint are those numbered accordingly. For example the C5-6 ZJ is supplied by the C5 and C6 medial branches. Because there are eight cervical spinal nerves, the C7-T1 ZJ is supplied by the C7 and C8 medial branches. Then from T1-2 downward the medial branches that supply the thoracic and lumbar ZJs are numbered one less than the corresponding joint. Thus, for example, the T1-2 ZJ is supplied by the C8 and T1 medial branches, the T8-9 ZJ by the T7 and T8 medial branches and the L4-5 ZJ by the L3 and L4 medial branches. To reduce confusion in the designation of ZJs and medial branches the International Spine Intervention Society (ISIS), which sets standards of practice and publishes practice guidelines for spinal interventions, has established a convention for denoting joints by the use of a hyphen (e.g., the left L4-5 ZJ) and denoting nerves by the use of a comma (e.g., the L3,4 medial branches).16 This convention is recommended for use in all written records. The medial branches lie close to the bone of the joint partners and are mostly bound down to it by fascia. Over the medial branches are the deep layers of the paraspinal muscles. The anatomic relationships of the nerves to the bones vary with the morphology of the cervical, thoracic, and lumbar regions. Generally speaking, the cervical medial branches run obliquely across the 357

358  Spine

The nerve supplies of the atlantooccipital and LAAJs are different from those of the ZJs. The atlantooccipital joints are supplied by the C1 nerve roots via their ventral rami, which follow curved courses around the outside of the arch of the atlas on each side.17 The LAAJs are supplied by the C2 spinal nerves, each of which lies immediately behind the LAAJ on that side bound to its inferior joint partner (the superior articular process of the axis) by fascia.17 The C2 spinal nerve divides behind the LAAJ into its ventral and dorsal rami; the ventral ramus passes across the back of the joint where it receives articular branches that form the LAAJ’s sensory supply; the dorsal ramus passes inferiorly and posteriorly, and its dorsal root ganglion lies behind the medial aspect of the lower part of the LAAJ.18 Another important anatomic relation of the LAAJ is the vertebral artery which lies immediately beside the joint’s lateral margin.

Biomechanics Figure 36-1  Lateral diagram of the upper spine from the first cervical (C1) vertebra down to the first thoracic (T1) vertebra showing the position of the zygapophysial joints. The needle tip indicates the C5-6 zygapophysial joint. (From Bogduk N: Back pain: Zygapophyseal blocks and epidural steroids.   In Cousins MJ, Bridenbaugh PO (eds): Neural Blockade in Clinical Anesthesia and Management of Pain, 2nd ed. Philadelphia, JB Lippincott, 1988, pp 935-954, with permission.)

waists of the articular pillars of the joint partners to the intervertebral foramina where they join the dorsal rami. The thoracic and lumbar medial branches run obliquely across the articular pillars and over the tops of the transverse processes of their vertebrae. The courses of the medial branches will be considered in more detail in the later sections on medial branch blocks. The nerve supply of the C2-3 ZJ is somewhat different. It is supplied by a single nerve, the medial branch of the dorsal ramus of the C3 spinal nerve, which is known anatomically as the third occipital nerve. It runs more or less horizontally across the joint to the C2-3 intervertebral foramen. The facets of the ZJs have surface areas of about 100-160 square mm. Their surfaces are curved and their anatomic orientations vary with the morphology of the cervical, thoracic, and lumbar regions. The orientations and their functional significance in each part of the spine will be considered in the section on biomechanics. As stated above, the joints properly termed zygapophysial are those of the twenty-three spinal motion segments from C2-3 down to L5-S1. Above C2-3 are the two uppermost spinal segments designated C0-1 and C1-2. The anatomy of those segments is specialized and their synovial joints that correspond to the ZJs lower down are designated by their anatomic joint partners, as the atlantooccipital joints (at C0-1) and the lateral atlantoaxial joints (at C1-2). These joints are also paired, with a left and a right joint at each level. The atlantooccipital joints involve two superior articular processes of the C1 vertebra (also called the atlas) which have concave facets that articulate with the convex facets of the occipital condyles of the base of the skull. The atlantoaxial joints, between the C1 vertebra (or atlas) and the C2 vertebra (the axis) are actually three in number. Anteriorly is the median atlantoaxial joint, a single synovial trochoid joint in which the odontoid process (or dens) of the axis rotates between the anterior arch of the atlas (in front of it) and the cruciate ligament (behind it). The lateral atlantoaxial joints (LAAJs) are paired synovial joints, one on each side, between the inferior articular processes of the atlas and the superior articular processes of the axis.17

The structure and function of the spine give the trunk of the body stability and mobility. Both the stability and the mobility of the spine are mediated largely by the ZJs. Stability is achieved by the way the individual vertebrae fit together at both interbody and ZJs to form a stable vertebral column. Stability is enhanced by four curvatures of the vertebral column in the sagittal plane, alternating extension curvature or lordosis (in the cervical region), flexion curvature or kyphosis (in the thoracic region), extension curvature (in the lumbar region) and flexion curvature (in the sacrococcygeal region). These curvatures give the spine (and hence the trunk) their characteristic static posture. Mobility of the spine is achieved primarily by the ways in which the ZJs move so as to make each pair of adjacent vertebrae a spinal motion segment. Every individual ZJ has the potential for the movements of translation (or gliding) and rotation in each of the three main anatomic planes—the sagittal, coronal (or frontal), and horizontal (or transverse) planes.19 Some of the six potential movements of each joint can only be achieved passively but all contribute to the mobility of the motion segment. The mobility of the spine as a whole is augmented by the ways in which the various spinal motion segments move in relation to each other giving the vertebral column ranges of extension and flexion in the sagittal plane, left and right side-bending in the coronal plane (also called lateral bending) and left and right rotation in the horizontal plane (also called axial rotation). The shapes and orientations of the facets of the ZJs determine their contributions to stability and mobility. The typical cervical ZJs have surfaces that are more or less flat with a slight curvature so that from the side the upper facet looks slightly concave and the lower one slightly convex; the cervical joints are oriented at 90 degrees to the sagittal plane and at angles of about 45 degrees to both the coronal and horizontal planes so that the upper facet of each (that on the inferior articular process of the upper vertebra) faces forward and downward,19,20 as in Figure 36-2. The facets of the thoracic ZJs are almost flat and oriented at an angle of about 20 degrees to the coronal plane. In this orientation, the upper facet of each faces forward,19,20 as in Figure 36-3. The lumbar ZJs have correspondingly curved surfaces so that the upper facet of each is concave and the lower facet that matches it is convex. The lumbar joints are oriented mainly in the sagittal plane so that the concave upper facet faces laterally and slightly anteriorly, and the convex lower facet faces medially and slightly posteriorly,19,20 as in Figure 36-4.

Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment  359

+45

–45

−45

−45

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Figure 36-2  Orientation of the articular facets of a typical cervical ­zygapophysial joint. (From White AA III, Panjabi MM: The basic kinematics of the human spine. A review of past and current knowledge. Spine 1978;3:12-20, with permission).

Y

0 0

–2

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–90

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36

Y

Y

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Z Figure 36-3  Orientation of the articular facets of a typical thoracic ­zygapophysial joint. (From White AA III, Panjabi MM: The basic kinematics of the human spine. A review of past and current knowledge. Spine 1978;3:12-20, with permission).

The cervical spine is the most mobile of the spinal regions because of its articular shapes and orientations, and the laxity of its joint capsules. The ranges of active movements of the cervical spine have been measured as up to 70 degrees each of extension and flexion (as determined by a radiographic study21), about 45 degrees of side-bending to each side and up to 40 degrees of rotation in either direction (as determined by a study using electric goniometers22). The ranges of side-bending and rotation are “coupled” so that they occur together, and to the same side, in the lower cervical spine (from C3 to C7; e.g., right side-bending is accompanied by right rotation). The passive ranges of cervical spinal movement have been measured as about 10 degrees more than the active ranges quoted in extension, flexion and side-bending to either side, and up to 50 degrees more in rotation to either side.23 Active and passive ranges of movement decrease as age increases.23 The movements of extension and flexion, side-bending, and rotation of each spinal motion segment occur around a central point known as the instantaneous axis of rotation (IAR).24 The position of the IAR in the segment determines the way the facets move in relation to each other as a ZJ goes through a range of movement. The positions of the IARs of cervical ZJ segmental motion have been determined—for example, the IAR of physiologic segmental extension in the cervical spine is located in the lower vertebral body of the segmental pair, near its upper end plate.24-,26 Stability is provided in the cervical spine by the shapes of the vertebral processes: the uncinate processes prevent lateral

Figure 36-4  Orientation of the articular facets of a typical lumbar ­zygapophysial joint. (From White AA III, Panjabi MM: The basic kinematics of the human spine. A review of past and current knowledge. Spine 1978;3:12-20, with permission.)

translation of the vertebral bodies and limit side-bending; the spinous processes limit extension. Further stabilization is provided by the spinal ligaments, the anterior longitudinal ligament (which limits extension), and the posterior longitudinal ligament, ligamentum flavum, and ligamentum nuchae (which all limit flexion). The thoracic spine is much less mobile and more stable than the cervical and lumbar spinal regions. The stability of the thoracic spine is enhanced by the coronal orientation of its ZJs, lesser degrees of laxity of their capsules, the supporting spinal ligaments, closer interlocking of the thoracic vertebrae, their long spinous processes, and the buttressing effect of the rib cage. The ranges of movement of the thoracic spine are difficult to measure experimentally in living subjects because the overlying ribs inhibit dynamic radiographic studies. A post mortem study of 10 specimens yielded an average range of about 60 degrees in the sagittal plane (i.e., of extension and flexion combined).27 The ranges are hard to discern clinically and in clinical practice the ranges of movement of the thoracic spine are usually assessed in conjunction with those of the lumbar spine.28 The ranges of active movements of the lumbar spine have been measured as up to 15 degrees of extension and 50° of flexion (as determined by several radiographic studies29-31), about 20° of sidebending to each side and up to 10 degrees of rotation in either direction.31,32 The movements of side-bending and rotation are coupled so that they occur together, and to opposite sides, in the upper lumbar spine (from L1 to L4); e.g., left side-bending is accompanied by right rotation in those motion segments.32 Side-bending and rotation occur to the same side in the L5-S1 segment and either way at L4-5 in different individuals.32 Extension and flexion also tend to be coupled with side-bending and rotation in the lumbar spine, but to varying extents in different subjects so that the coupling is much less predictable.32 As in the other spinal regions, the active ranges of lumbar movement decrease with increasing age.33,34 In the lumbar spine, as elsewhere, the movements of extension and flexion, side-bending, and rotation of the spinal motion segments each occur around an instantaneous axis of rotation (IAR). The positions of the IARs in the lumbar spine have been determined so, for example, the IAR of physiologic extension and flexion of a typical lumbar motion segment is located on the upper end plate of the lower vertebra of the segmental pair.35 The lumbar spine is stabilized by the mainly sagittal orientation of its ZJs (which limits side-bending and rotation), relatively taut ZJ capsules (compared to those of the cervical region), the anterior longitudinal ligament (which limits extension), the posterior

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longitudinal ligament, ligamentum flavum, and interspinous ligaments (which all limit flexion) the intertransverse and iliolumbar ligaments (which limit side-bending), and by the spinous processes (which limit extension). The resultant stability of the lumbar spine enables it to support the weight of the upper body in various postures at rest and during movements. Kinetics is the domain of biomechanics that deals with loading of anatomic structures in static and dynamic situations. A loading force, technically called a stress, affects a structure to which it is applied and tends to deform or damage it. The structure reacts to the stress by developing a change technically called a strain, a change for example of length and/or of internal tension, which helps the structure to resist the stress. If the stress is excessive, beyond the capacity of the structure to resist it, damage will occur. Static loading of the cervical spine is caused by the weight of the head and the tensions in cervical ligaments and muscles. The static load varies with posture; for example, it is low in lying with the head and neck supported, higher in upright sitting with the head and neck in the anatomic (neutral) position, and higher still with the head and neck at the end-ranges of extension and flexion.36 Dynamic loading of the cervical spine includes the component of static loading plus the effects of forces applied by movement. Internal dynamic loading occurs during active bodily movements that involve postural changes of the head and neck. External dynamic loading occurs as the result of passive applications of force to the head and neck. External loading occurs in circumstances that involve acceleration or deceleration, or when there is impact between the head or neck and an object. For instance, internal dynamic loading of the cervical spine occurs during physiologic movements of the neck through any range. Additionally, external dynamic loading may occur due to impact with a moving object or with the ground (as in a fall) or due to the gravitational effects of rapid acceleration or deceleration (as in a motor vehicle accident). Static loading of the thoracic and lumbar spines results from the weight of the upper body, the tensions in thoracic and lumbar ligaments and muscles, and the effect of any additional load such as an object held in the hand. As in other spinal regions, static loading varies with posture. Lumbar static loading is relatively very low in supported supine lying, quite low in relaxed upright standing, higher in relaxed upright sitting, and progressively higher in standing with lumbar flexion and sitting with lumbar flexion.37 Dynamic loading of the thoracic and lumbar spines is a combination of static loading and any additional force(s) caused by active bodily movement or by the passive effects of loads applied with movement from external sources. For example, during ordinary walking, the dynamic loading of the lumbar spine varies with the phases of the gait cycle and is greatest at toe-off.38 In lifting an object while standing, dynamic loading of the lumbar spine is greater if the lumbar spine is flexed than if the back is kept straight, because the flexed position involves additional moments of force related to the distances of the upper body and the lifted object from the center of gravity.39,40

Zygapophysial Joint Pain Mechanisms Pain is defined “as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”.41 The unpleasant emotional experience is

mediated by unpleasant sensation, which begins with stimulation of sensory fibers of the peripheral nervous system. Peripheral sensory nerves have Ad and c nerve fibers that are sensitive to pain. Ad and c fibers are polymodal: they are sensitive to touch, vibration, proprioception, and thermal change as well as pain. In their role as pain sensors they are called nociceptors and the neurologic process of encoding and processing noxious stimuli which evoke pain is called nociception.42,43 ZJs have afferent sensory innervation including Ad and c fibers and so are capable of generating pain.5,15 Both the synovium and the capsule of each ZJ are richly supplied with nociceptor terminals. When they are stimulated in certain ways, pain will be generated from that joint. Pain generation was demonstrated in a study of normal volunteers; when ZJs were distended by injections of contrast medium, pain was evoked in patterns of distribution that were found to be reliable, recognizable, and joint-specific.12 Thus, the neurophysiologic mechanism of ZJ pain is that painsensitive afferent nerve terminals in the joint’s tissues are activated by the effect of a noxious stimulus that begins the process of nociception. The initial activation of sensory afferents is called transduction. After it occurs, the resultant nociceptive signal is transmitted via the pain pathways of the peripheral and central nervous systems to the cerebral cortex where it is interpreted as the experience of pain. The pathologic mechanism of ZJ pain (the stimulus that triggers the neurophysiologic process) is usually mechanical. Force (stress) applied to a joint produces a change in the mechanical state (strain) of the joint components. Such strains may actually damage joint tissues and alter the mechanical function of the joint, or may only threaten tissue damage, as capsular distention does. Whether they cause actual or potential tissue damage, such mechanical changes act as noxious stimuli to activate Ad and c fiber terminals. The types of mechanical changes that do this are considered under the next two headings.

Etiology The unpleasant experience of pain begins with sensation that the brain interprets as actual or potential tissue damage.41 ZJ pain is initiated by mechanical loading of the tissues of one or more ZJ(s) at levels close to, or beyond, their load-bearing capacity. In such circumstances, the joint tissues are strained as the load is applied and if the load exceeds their capacity to resist, they will fail. In both phases of strain and then failure, nociceptors are stimulated, evoking pain. The circumstances in which such loading occurs include any in which the posterior elements of the spine are subjected to damaging forces. The more common situations in which such forces are applied include motor vehicle accidents, industrial accidents, and falls. In these events, the tissue damage results from a single application of destructive force. Damage can be caused by repeated applications of force over time—but if so, the forces must be substantial. There is no evidence that ZJ pain is caused by posture or by repetitive use of muscles, and there is abundant evidence that ZJ pain is not caused by the universal changes of spondylosis (see later under “Diagnosis of Zygapophysial Joint Pain”). The damaging forces that occur in motor vehicle accidents have been studied most. A cineradiographic in vivo study of cervical ZJs under loading in a simulated rear-end collision44 showed that under accident conditions the instantaneous axis of rotation moved upward and forward from its normal position in the lower vertebral

Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment  361

36

body of a spinal motion segment to a position in the upper vertebral body of the pair. Movement around this “crash IAR” caused the ZJ facets to clash in unusual ways—often so that the posterior edge of the upper facet gouged into the surface of the lower facet. Other phenomena observed included the upper facet making impact on the anterior edge of the lower facet with shearing and compressive forces on both, and the facets gliding to different extents causing rupture of the joint restraints. Another study using human cadaver head-neck complexes subjected to simulated motor accident conditions45 produced similar findings. The effects observed were consistent with what has been found in studies of the pathology of ZJ injuries, as set out in the next section.

Pathology Several pathoanatomic studies have been undertaken to investigate the consequences of spinal structures being subjected to excessive forces.46-54 These studies have been based on post mortem examinations, some from autopsies conducted on individuals who had died in circumstances likely to have injured their spines, and some from autopsies conducted on those who died in other circumstances but were known to have had spinal pain from injuries sustained previously, some many years before death. Most of the studies also included radiologic examination of the spine to investigate any relationship between pathoanatomic findings and radiographic appearances. In the cervical spine, these studies showed that injuries of the cervical ZJs and interbody joints are common consequences of spinal trauma but many of the injuries found involved only the soft tissues of the joints and were undetected by plain radiography.48,50-53 In one study of 22 spines, 19 (86%) were found to have ZJ injuries, many of which were at multiple levels. Sixty-nine injured ZJs were observed; of these only three subjects (14% of the study population) were found by radiography to have ZJ injuries, and in each case, only one ZJ injury was detected radiographically. So of the 69 injuries observed at autopsy, 66 (96%) went undetected by radiographic studies.50 In another study of 45 spines from people who died in motor vehicle accidents, the investigators found soft tissue injuries of the cervical ZJs in 72% of the sample but identified fractures in only 28% of them.51 The results of the other studies were similar. Studies of the cervical spines of those known to have suffered chronic neck pain and to have died in circumstances requiring autopsy (but unrelated to neck trauma) showed lesions in the cervical ZJs consistent with the long-term effects of the types of injuries observed in acute cases.51 The cervical ZJ pathology observed in these studies was predominantly of soft tissues, which explains why most lesions were not detected by radiographic imaging. A range of pathologic lesions was found, including tears, splits, and partial loss of articular cartilage. In some cases, the full thickness of the articular cartilage was gouged away and this was often associated with injury of the surface layers of the subchondral bone (termed infraction), a lesion obvious on direct visualization or by special staining on microscopic preparations but not of such depth as to deform the bony surface grossly, so not detected radiographically. An example of full-thickness cartilage loss and infraction is shown in Figure 36-5. Other lesions observed included tearing of ZJ capsules and small undisplaced fractures of facet tips or of articular processes which did not appear on radiographs. In the chronic cases, the spines of those who had suffered spinal pain and died later of some other

Figure 36-5  An example of acute zygapophysial joint injuries observed at autopsy: acute articular cartilage lesion of gouging type, with infraction of the inferior facet of a cervical zygapophysial joint. (Image courtesy of Prof. James Taylor of Western Australia.)

cause, pathologic changes observed included distortion of the joint surfaces with thinning of the articular cartilage and disruption of the articular cartilage.51,53 In the atlantooccipital and LAAJs, the pathologic lesions found were again mainly of articular soft tissues, the articular cartilages, and joint capsules. Also observed in conjunction with some soft tissue injuries at these levels were undisplaced fractures of the anterior and/or posterior arches of the atlas, of the odontoid process (or dens), and/or the arches of the axis.51,54 Pathoanatomic autopsy studies of the lumbar spine show that injuries of the lumbar ZJs are common consequences of spinal trauma as well. Again many of the injuries observed on dissection involve only the soft tissues of the joints and are undetected by plain radiography. In one study of 31 lumbar spines of individuals killed in motor vehicle accidents or other traumatic circumstances, 24 (77%) were found to have ZJ injuries, many of which involved more than one ZJ. Healed injuries of similar types were found in the spines of others who died of other causes but had been known to have a history of lumbar spinal pain since previous accidents. As in the studies of cervical injuries,48,50-54 few of the acute or chronic lumbar injuries were detected by plain radiography.47 Other studies have shown such injuries are not detected reliably by more sophisticated imaging modalities either (see later, in the section “Diagnosis of Zygapophysial Joint Pain”). The lumbar ZJ pathology observed in the autopsy studies was also predominantly of soft tissues, which again explains why lesions were not detected by radiologic examination. The pathologic lesions found in lumbar ZJs were similar to those described in the cervical region: tears, splits, and gouging away of articular cartilage, infraction of subchondral bone (Fig. 36-6), tearing of joint capsules, and small undisplaced fractures of facet tips or of articular processes that did not show radiologically. In the spines of those who died after suffering lumbar spinal pain for a long time, pathologic changes observed in the ZJs included thinning of the articular cartilage, irregularity of the joint surfaces, and disruption of the joint capsule.47,49,51

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in Western countries,71 42% in the rural population of Tibet,70 60% among Finnish reindeer herders,72 and from 60% to 83% among rural workers in China.73 The prevalence of lumbar ZJ pain has been determined as 30% to 40% among adults with chronic back pain in the United States.55,74 Age-related prevalences of lumbar ZJ pain have been measured in Australia, in studies based on definitive diagnosis by criterion standard methods, as 15% of younger adults with a history of injury and attending a pain clinic75 and 40% of older adults attending a rheumatology clinic.76 Both these studies showed the L5-S1 level is most commonly affected in the lumbar region, and the L4-5 level is the next most commonly affected.

Diagnosis of Zygapophysial Joint Pain

Figure 36-6  An example of lumbar zygapophysial joint injuries observed at autopsy: infraction of the inferior facet of a lumbar zygapophysial joint with organization of the subchondral bone (arrow). (Image courtesy of Prof. James Taylor of Western Australia)

Epidemiology ZJ pain is common. It is one of the more common causes of spinal pain related to the neck, upper back, or lower back, and must be considered as a diagnostic possibility whenever a patient presents with any such symptom.55 The prevalence of acute spinal pain is unknown because many acute conditions are of brief duration and so do not reach the threshold for inclusion in studies. Although the prevalences of acute cervical, thoracic, and lumbar ZJ pain are unknown, inferences can be drawn from data that are available for the prevalences of chronic cervical, thoracic, and lumbar ZJ pain. The 12-month prevalences of chronic neck pain in the general adult population have been assessed as 1.7% (for more intense chronic neck pain that limits ability to work), 2.4% (for chronic neck pain that limits social activities), and 11.5% (for chronic neck pain that limits some activity).56 Studies show the prevalence of cervical ZJ pain among patients with chronic neck pain after motor vehicle accidents or similar trauma is at least 50%55-59 and in some circumstances may be as high as 80%.60 In those with lower neck pain the C5-6 level is most commonly affected and C6-7 is the next most commonly affected.58 Among patients whose dominant symptom after a motor vehicle accident is headache, the prevalence of pain stemming from the C2-3 ZJ has been assessed as between 37% and 68% with a mean of 53%.61,62 Chronic upper back pain related to the thoracic spinal region has been estimated to have annual prevalences in adult populations of between 5% and 10%.63,64 The prevalence of chronic thoracic ZJ pain among those with thoracic spinal pain has been determined as 48%.64 Chronic low back pain is very common in all countries. The point prevalence of chronic low back pain in general adult populations has been estimated as about 10% in Western countries such as Australia,65 New Zealand,66 the United Kingdom,67,68 and the United States69 and as high as 34% in the rural population of Tibet.70 The annual prevalence has been reported as between 13% and 49%

ZJ pain can be diagnosed definitively, using tests that are specific and minimally invasive. Before proceeding to order (or perform) such tests on a patient with chronic spinal pain, the clinician should decide whether testing for ZJ pain is the priority, or whether other sources of pain should be investigated first. That decision will rest on a clinical impression and on the known epidemiology of the various causes of chronic spinal pain. Clinical assessment, taking the medical history and performing a physical examination, may help the clinician to form an impression of the likely cause of a patient’s pain and should be carried out carefully and systematically in every case.77,78 However, there are no clinical features that are pathognomonic of ZJ pain at any ­spinal level, so the decision to test for ZJ pain cannot be validated on clinical grounds alone. Some impression can be gained of the likelihood of a ZJ being the source of a patient’s pain by an informed consideration of the symptoms, and especially of the pain distribution and pain ­quality.77 The distribution of pain generated from a particular structure is called a “pain map.” Studies based on joint provocation in normal subjects and anesthetization of specific joints in those with chronic pain have resulted in pain maps being plotted for ZJs at all cervical,12,79-81 thoracic,82 and lumbar4,83-85 levels, and for the atlanto­ occipital and LAAJs.86,87 The quality of pain provides another useful clue. ZJ pain is typically dull and aching in quality, of the type called somatic pain (in a local distribution near the source) and somatic referred pain when it is perceived in more distant regions.88,89 Other spinal structures may also generate somatic pain, so it is not specific to ZJs, but it is quite different from radicular pain, the sharp, shooting, and sometimes “electric” pain associated with nerve root irritation.90 The pain maps of cervical ZJs are depicted in Figure 36-7. If a patient presents with somatic and/or somatic referred pain in the neck, in the lower neck and shoulder, or in the upper neck and head (so-called cervicogenic headache91,92) in a distribution like one of those described in Figure 36-7, it may be suspected to be of cervical ZJ origin. The pain maps provide clues to the level of a joint that may be a pain source but do not identify a level specifically because the maps overlap considerably: each part of a patient’s neck lies in at least two, and perhaps as many as four, of the areas to which pain may be referred from particular joints. When a patient presents with what is suspected to be cervicogenic headache, the lateral atlantoaxial (C1-2) and atlantooccipital (C0-1) joints must also be considered as possible sources. The pain maps of those joints are depicted in Figures 36-8 and 36-9. The pain maps of the C0-1, C1-2, C2-3, and C3-4 joints also overlap considerably, so although they provide clues to the possible origin of

Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment  363

36 C2–3 C3–4 C4–5 C5–6 T1

C6–7

Figure 36-7  Pain maps showing patterns of distribution of cervical zygapophysial joint pain stemming from the C2-3 to the C6-7 levels. (From Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint pain patterns: I: A study in normal volunteers. Spine 1990;15:453-457, with permission.)

Figure 36-9  Pain map showing the pattern of distribution of atlantooccipital (C0-1) joint pain. (From Dreyfuss P, Michaelsen M, Fletcher D: Atlanto-­ occipital and lateral atlanto-axial joint pain patterns. Spine 1994;19:11251131, with permission.)

T1 T3–4

T4–5 T1

T5–6

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T8–9

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Figure 36-8  Pain map showing the pattern of distribution of lateral atlantoaxial (C1-2) joint pain. (From Dreyfuss P, Michaelsen M, Fletcher D: Atlanto-occipital and lateral atlanto-axial joint pain patterns. Spine 1994;19:1125-1131, with permission.)

cervicogenic headache, they do not, in themselves, enable identification of the source. In the thoracic spinal region the pain maps overlap as well. The distribution of pain from a thoracic ZJ is to an adjacent zone of the upper back, lateral to the joint and from half a spinal segment higher to a full segment lower as shown in Figure 36-10. Lumbar ZJ pain maps are comparable. Somatic pain from a lumbar ZJ occurs in an adjacent zone of the lower back, lateral to the joint, and from about one spinal segment higher to one segment

Figure 36-10  Pain maps showing patterns of distribution of thoracic zygapophysial joint pain. (From Dreyfuss P, Tibiletti C, Dreyer SJ: Thoracic zygapophyseal joint pain patterns. A study in normal volunteers. Spine 1994;19:807-811, with permission.)

lower, with somatic referred pain extending down the back of the leg. The patterns overlap to a considerable extent with each joint generating pain to a slightly lower level than that of the joint above it. The overlap makes it difficult to depict individual maps in a single diagram but the composite pattern of distribution is as shown in Figure 36-11.

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Figure 36-11  Pain map showing patterns of distribution of somatic and somatic referred pain of lumbar zygapophysial joint origin. (From Bogduk N, McGuirk B: Medical management of acute and chronic low back pain: an evidence-based approach. Amsterdam, Elsevier, p 9, 2002, with permission.)

The mode of onset is another feature of the history that may suggest a patient’s pain is of ZJ origin. Because ZJ pain is generally due to injury, its onset is usually related to a traumatic event such as a motor vehicle accident, an industrial accident, a mishap while playing sport, or a fall. When a patient describes the onset of their pain as immediately after such an event, or in the day or so afterward when soft tissue hemorrhage, contusion, and edema develop, there is likely to be a causal relationship between the event and the pain. ZJ injury may be suspected but other structures must also be considered as possible pain sources. If a patient has pain that does not seem to be associated with any traumatic event, ZJ injury is less likely to be the cause of the problem. It should not be excluded as a diagnostic possibility, as the causative event may have been forgotten or it may not be associated with the pain in the patient’s mind because of what they may have been told earlier. Physical examination is a traditional component of clinical assessment and it is valuable for helping the clinician develop an impression of the patient and the problem. However, clinical examination findings provide few clues to the likelihood of pain being of ZJ origin and there is no physical sign, or combination of signs, that enables identification of a particular ZJ as a source of pain. By convention, physical examination of the musculoskeletal system includes inspection, palpation, and testing of movements (which includes assessing active, passive, and accessory ranges of movement, and challenging the restraints to movement).78 If the clinician examines the patient systematically and addresses all these domains, many signs will be elicited but care must be exercised in

interpreting them in the light of the scientific evidence of their reliability and validity. Data on the reliability of inspection of the various regions of the spine for lordosis, kyphosis, and scoliosis show interobserver agreement to be low, with Kappa scores from 0.13 to 0.39.93,94 Data on the reliability of palpation of the spine for tenderness at specific sites also show interobserver agreement to be low, with Kappa scores from 0.11 to 0.53.95-97 The reliability of assessing gross ranges of active spinal movement seems somewhat better, in some ranges at least, with, for example, reported Kappa scores of 0.40 for cervical rotation and 0.56 for cervical extension,95 from 0.35 to 0.74 for lumbar extension,94 but only from 0.11 to 0.43 for lumbar sidebending.94 The reliability of testing passive intervertebral movements is very poor, with Kappa scores in negative ranges.93,98 Reliability is one thing but reliability data only show the consistency of observations, not what those observations can be interpreted to mean. Such interpretation must be based on evidence of validity. There is very little evidence of the validity of physical examination in the diagnosis of ZJ pain. There are no sound data on the validity of inspection or testing gross ranges of movement in the diagnosis of ZJ pain in the cervical, thoracic, or lumbar regions. There are no sound data on the validity of palpation in the diagnosis of thoracic or lumbar ZJ pain. Such data as exist on the validity of physical examination relate to palpation for specific physical signs in the assessment of patients with neck pain. There are data99 showing certain physical tests are valid, with positive likelihood ratios of from 2.7 to 12.8, for confirming that pain is of spinal origin but not for identifying the specific source of that pain. The data from two validity studies show that manual examination is not valid for diagnosis of cervical ZJ pain. A small set of data from a preliminary study100 seemed to show that manual examination was valid for the identification of a painful cervical ZJ and much faith was placed on that evidence by manual therapists for some time thereafter. However, the data set was small and the authors of that early study called for further research to be done before their results were generalized. In response to that call, a larger study101 was done and its results showed clearly that manual examination is not valid for the diagnosis of cervical ZJ joint pain; the positive likelihood ratios were only from 1.4 to 1.8. Reassessment of the data of the earlier study, in the light of later knowledge of aspects such as the rate of false-positive results, showed the results of both studies are consistent and both actually show manual examination is invalid for the purpose. The summary of the evidence on clinical assessment is that some guidance is provided by established patterns of distribution of pain from individual joints, the so-called spinal pain maps, but there are no clinical methods that are valid for identifying specific painful ZJs. Imaging studies provide information about the spine and traditionally imaging has been used in the assessment of patients with spinal pain, but imaging results do not identify painful spinal joints. The imaging modalities used most often are plain radiographs, computer assisted tomographic (CAT or CT) scanning, magnetic resonance imaging (MRI), and isotopic bone scans. These frequently show radiologic appearances of spondylosis or osteoarthrosis, including joint space irregularity and narrowing, subchondral bony sclerosis, subchondral cysts, periarticular bony hypertrophy, and the presence of osteophytes. These changes, sometimes incorrectly called “degenerative changes,” reflect the normal responses of the articular cartilage and the subchondral bone to the repeated biomechanical stresses of daily living.102,103 It is often assumed that there is a causal relationship between these imaging changes and

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pain generation but the scientific evidence suggests otherwise. The fact that the changes are age-related is clearly demonstrated by the results of numerous studies showing direct correlation between their prevalence and increasing age.104-109 The fact that they are not regularly associated with pain is borne out by the results of numerous studies showing no correlation between the presence of pain and spondylotic changes shown by plain radiography,110-116 CT scanning,117 and MRI.118-121 No other radiologic appearances seen on plain radiography,122,123 CT scanning,124 MRI,125,126 or any other imaging modality have been proved to be correlated with ZJ pain. Thus, after comprehensive clinical assessment and imaging, the clinician may gain the impression that a patient’s pain may be of ZJ origin, but that impression cannot be confirmed by clinical features and/or imaging results—separately or in combination. The only way of determining that a ZJ is (or is not) a source of pain is to test it by anesthetic blockade of that joint alone, to see if the pain is abolished by the blockade: such tests are called diagnostic joint blocks. If a decision to undertake ZJ blocks is made, the next issue is which joint to test first. That decision will depend on the clinical impression; further guidance may be obtained from the prevalence data set out earlier under “Epidemiology”. As stated there, in the cervical spine, the ZJs most often involved in cervicogenic headache are those at the C2-3 level58 and the joints most often associated with lower neck pain are those at C5-6.62 There are no prevalence data for specific segmental origins of thoracic ZJ pain. In the lumbar spine, the ZJs most often involved in pain generation are those at the L5-S1 level.75

Indications for Interventions Interventions that may be employed in the management of any type of pain include diagnostic interventions and therapeutic interventions. Their indications are determined accordingly and may be considered as general and specific. The general indications for any diagnostic intervention are three in number and all three must be satisfied on every occasion. A diagnostic intervention is indicated if, and only if, (1) the patient is likely on the basis of their clinical presentation to have a particular condition, (2) the intervention is known to be useful for determining whether that condition is present or not, and (3) the intervention is justified in the patient’s circumstances. The first of these relates to clinical features which are discussed earlier in the section on diagnosis. The second relates to the validity of the intervention which will be discussed later in the chapter, under the headings for each specific procedure. The third general indication relates to matters of safety, utility, cost-effectiveness, and ethical considerations. The main safety issues are concerned with the patient’s general health and whether the intervention is likely to affect any other medical condition they may have. Utility involves both therapeutic utility (whether the results of the diagnostic intervention will lead to effective treatment), which will be discussed in the sections on validity, and personal utility (whether the outcome of the intervention will be helpful to the patient in enabling them to understand the condition and cope with it). Cost-effectiveness is a matter of whether the costs of the intervention, including the cost of the investigative procedure itself and other costs related to the patient having access to it, are justified by the value of the results in the management of the condition. The ethical considerations are those concerned with informed consent. Before a patient has any intervention, they should be fully informed about its purpose, the

technique to be used, what they can expect while undergoing the procedure, and all associated risks. Having received this information, preferably in printed form as well as verbally, the patient must give informed consent in writing before each investigative procedure is undertaken. The general indications for therapeutic interventions are somewhat similar. A therapeutic intervention is indicated if, and only if, (1) the patient has been diagnosed definitively as having a condition for which the intervention is applicable, (2) the intervention is known to be effective for the treatment of that condition, and (3) the intervention is justified in the patient’s circumstances. The first of these relates to diagnostic validity which will be discussed later in the chapter, under the headings for each specific diagnostic procedure. The second relates to the validity of the therapeutic intervention itself which also will be discussed later in the chapter, under the headings for each specific therapeutic procedure. The third general indication again relates to matters of safety, utility, and cost-effectiveness, and ethical considerations: these are much the same as described for diagnostic interventions. When contemplating specific indications for interventions in the management of ZJ pain, the first consideration is the duration of the condition. By convention, conditions are classified by their time courses as acute and chronic.127 Acute pain is defined as that of short duration which is likely to settle spontaneously by natural healing of the causative condition. Chronic pain is defined as that which persists beyond the normal time of natural healing.128,129 After much discussion among clinicians and researchers about how long should be allowed for natural healing, acute pain was defined as pain present for up to 3 months and chronic pain was defined as pain present for more than 3 months.130 Thus acute and chronic pain differ fundamentally in that the former is likely to resolve spontaneously by natural healing, whereas the latter is not. Accordingly, the rational management of acute spinal pain is quite different from that of chronic spinal pain. Unfortunately for many pain sufferers, the difference is apparently not appreciated by some clinicians and acute spinal pain is often over-treated, whereas chronic spinal pain is often under-treated. Acute spinal pain, in most cases, will resolve by natural healing if just left alone.131-133 Clinicians who do not appreciate this phenomenon often use interventions to treat acute spinal pain when to do so is unlikely to shorten the course of the condition and may even lengthen it. Active interventions are actually contraindicated for most acute spinal pain. What patients with acute spinal pain need is explanation of the favorable natural history, reassurance, pain relief (by analgesic medication or some other method) and encouragement to remain active; beyond that all they need is follow­up until the pain settles.131-133 Chronic spinal pain usually persists until effective treatment is applied, so intervention is indicated in virtually every case. Some clinicians seem unaware of the evidence in this regard and manage chronic spinal pain as if its cause is unidentifiable and only general measures can be applied to help the patient live with the problem. That approach is outmoded. These days the causes of most chronic spinal pain can be identified precisely and many of those identifiable causes can be treated effectively. That is certainly the case for chronic ZJ pain. The key to the management of chronic spinal pain is precise diagnosis.134 The specific indications for a diagnostic intervention in the management of chronic ZJ pain are (1) the patient is likely on the basis of their clinical presentation to have chronic ZJ pain, (2) the intervention planned is known to be useful for determining

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whether ZJ pain is present or not, and if so from which joint(s), and (3) the intervention is justified in terms of its safety, therapeutic utility, personal utility for the patient and cost-effectiveness, and the patient has given informed consent. The specific indications for a therapeutic intervention in the management of chronic ZJ pain are (1) the patient has been diagnosed definitively as having ZJ pain, and the source(s) of that pain have been identified precisely, (2) the intervention is known to be effective for the treatment of the condition the patient has, when it is done in the manner planned, and (3) the intervention is justified in terms of its safety, therapeutic utility, personal utility for the patient and cost-effectiveness, and the patient has given informed consent.

Risks and Contraindications Risks associated with interventions used in the management of chronic ZJ pain can be considered as minor side-effects and more severe ones. Minor side-effects include vasovagal reactions (if the patient is anxious or afraid of needles), feeling needle-pricks, unsteadiness (due to effects on proprioceptive reflexes) and minor bruising. Prior information and reassurance before and during the procedure help to minimize any problems. After every block injection the patient should be reminded of the possibility of unsteadiness and warned not to engage in activities in which balance is important, such as walking on stairs and driving a vehicle, until the effect has worn off. More severe side-effects include major bruising, “rebound pain,” local anesthetic effects, inadvertent puncture of nontarget structures, inadvertent coagulation of nontarget nerves, ­allergic reaction and infection. Another important risk is exposure to ­ionizing radiation. The likelihood of bruising is increased if the patient is taking drugs such as anticoagulants, aspirin, and other nonsteroidal antiinflammatories. The risk can be reduced by suspending the drug or reducing the dose before a procedure but this must be done in ways that do not aggravate the condition for which the medication is being taken. Some patients who obtain relief after a procedure feel a “rebound” effect if/when the pain returns; that is, it seems worse at first then settles back down to the usual level. This may be because they did something they would not have done if the pain was present and patients should be advised not to do anything strenuous while a block is in effect. Local anesthetics used in interventions for pain may cause effects that range from numbness and weakness to more severe disturbance of balance and other bodily functions. If such effects occur, they will last only for as long as the local anesthetic is active, but in rare cases, they may require additional treatment to restore the functions affected. Other potential risks are allergy and infection; these risks can be minimized by careful history-taking prior to any intervention and attention to sterility during procedures. Inadvertent puncture of nontarget structures such as thecal membranes, nerve roots, and blood vessels may cause a variety of unwanted effects. Special risks associated with interventions that involve thoracic needling are pleural puncture and pneumothorax. Inadvertent coagulation of nontarget nerves is a potential complication of a thermal radiofrequency (RF) procedure done without due care in the placement of the electrode. All those risks are minimized by the operator having knowledge of spinal anatomy, including ranges of anatomic variations, and using careful technique. The possibility of such effects should be recognized and no matter how unlikely such eventualities may be, every procedure should be done in a facility for dealing with any complication that may arise.

Exposure to ionizing radiation should not be a major risk in spinal interventions because the patient dose of radiation will be very low if appropriate care is taken, including coning whenever possible and avoiding the use of continuous screening unless absolutely necessary. There is no safe dose of radiation and special consideration should be given if a patient is pregnant. Also, shielding should be considered for all premenopausal females having procedures in which the ovaries may be exposed to radiation. Contraindications for interventions in the management of chronic ZJ pain may be considered as absolute and relative. Absolute contraindications for interventions are if (1) the patient is unable or unwilling to consent to the procedure, or (2) the patient is unable to cooperate during the procedure, or (3) the patient has a definite history of anaphylactic reaction to any preparation to be used in the procedure, or (4) the patient has evidence of an untreated localized infection in the procedural field, or (5) the patient has a known bleeding diathesis that cannot be remedied to allow the procedure. Relative contraindications warn that the intervention should be undertaken only after careful weighing of the risks and potential benefits of the procedure, and then only with appropriate precautions. They are if (1) the prospective patient is allergic to any of the drugs that are to be administered, or (2) the patient has a suspected idiosyncratic reaction to nonionic contrast medium, or (3) the patient has a known systemic infection, or (4) the patient is currently medicated with anticoagulants, or (5) the patient is pregnant, or (6) the patient has anatomic derangements, congenital or surgical, likely to compromise the safe and successful conduct of the procedure. In the following sections several diagnostic and therapeutic interventions are described. Readers should note that these procedures are described here in sufficient detail to promote understanding of them but no more than that. The practice of interventional spine care requires detailed knowledge of regional anatomy, appreciation of radiologic anatomy and particular skills that can only be gained by proper practical training under the supervision of experienced spinal interventionists. This training can be gained in courses that are now widely available. No practitioner should attempt to perform any spinal intervention without such training and certainly not by simply following the descriptions and images in this chapter.

Medial Branch Blocks Development Medial branch blocks are local anesthetic blocks of the articular nerves (the medial branches) that transmit sensory information including nociceptive signals from ZJs (as described earlier under “Mechanisms”). Historically, the first method used to test a ZJ as a possible source of pain was injection of local anesthetic into the cavity of a lumbar ZJ84; such tests are called intraarticular blocks (IABs). Comparable techniques were developed for cervical135 and thoracic136 ZJs as well. Later, less invasive methods were developed to achieve blockade of a specific joint by blocking the articular nerve(s) outside the joint137,138; such tests are designated by the particular nerves involved as medial branch blocks (MBBs) and third occipital nerve blocks (TONBs). Because articular nerve blocks are less invasive and are performed more often to investigate the common sources of chronic spinal pain, they will be described first. Cervical Medial Branch Blocks C3 to C6—Procedure A cervical medial branch block procedure involves a lot more than the needling and injection commonly associated with the name. This is also true for other such procedures. Each diagnostic

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procedure involves three phases, a preoperative phase, an operative needling phase, and a postoperative observational phase. The full test process involves a fourth phase, the interpretation of individual block results and the integration of the information they provide in the overall process of diagnosis. If a medial branch block is thought of mainly as the needling part, the other phases may be given less emphasis than they deserve and the whole process may be compromised. A cervical medial branch block test is intended to determine whether a particular cervical ZJ is a source of pain. The test is designed to be specific, so initially, only one joint should be tested at a time. If the results of specific tests suggest that two or more ZJs may be involved in generating the patient’s pain, on a subsequent occasion the combination of joints may be tested together to see if they are all contributing to the pain in that region. Each cervical ZJ from C3-4 down to C6-7 is supplied by two medial branches, the medial branches of the cervical dorsal rami above and below the joint. Thus, the C5-6 ZJ is supplied by the C5 medial branch and the C6 medial branch. The procedure to test the C5-6 ZJ as a pain source involves blocking each of those two nerves. The courses of the medial branches have been plotted by cadaveric dissection studies and shown to lie more or less horizontally across the middle parts of the articular pillars that join the superior and inferior articular processes of each vertebra.139 The courses of these medial branches are illustrated in Figure 36-12. These nerves are the targets at which cervical medial branch blocks (MBBs) are aimed. The nerves themselves are not seen on fluoroscopy, but by appreciating the ranges of their courses it can be understood how particular medial branches can be anesthetized. They are accessible for injection around them as they pass over the “waists” of the articular pillars. Needles can be placed onto them at that site readily and safely from lateral approaches, as depicted in Figure 36-13. The target point for each MBB injection is the centroid or geometric center of the relevant articular pillar (Fig. 36-14). Medial branch blockade is achieved by placing the tip of a spinal needle at that point and injecting a small volume of local anesthetic, just sufficient to reach the highest and lowest of the known courses of the nerve in question. The volume of the injectate must be large enough

to achieve that coverage reliably but not so large as to spread to and block other nerves because that would compromise the specificity of the test. Local anesthetic preparations suitable for the purpose are lidocaine 2% or bupivacaine 0.5% and the volume of injectate sufficient to achieve the desired spread has been found to be no more than 0.5 mL.137 The placing of a needle tip at a specific point on the spine requires particular facilities and equipment. MBBs and other such procedures should be performed in a procedure suite or operating room where infection control measures are undertaken regularly. The patient’s safety is a prime consideration and it is crucial for safety that the operator knows precisely where the needle is at all times. The procedure must be done with radiologic guidance, preferably that provided by a fluoroscope with a high-resolution image intensifier and a C-arm that allows the X-ray beam to be directed at different angles to provide anteroposterior (AP), oblique, and lateral views without moving the patient. A radiolucent x-ray table is also required, preferably one with a mobile plinth that can be moved to modify the fluoroscopic views. Also needed in the procedure suite are spinal needles, extension tubes, and syringes for the block­injections, local anesthetic agents, sterile layouts on which the equipment for the procedure can be placed, skin preparation trays with swabs, forceps and suitable antiseptics, sterile drapes, sterile towels and sterile gloves for the operator, and a scrub sink adjacent.

ton a a mb mb

Figure 36-13  Target points for cervical medial branch blocks indicated by needles introduced via lateral approaches. (From Bogduk N: Back pain: Zygapophyseal blocks and epidural steroids. In: Cousins MJ, Bridenbaugh PO [eds]: Neural Blockade in Clinical Anesthesia and Management of Pain, 2nd ed. Philadelphia, JB Lippincott, 1988, 935-954, with permission.)

Figure 36-12  Plots of the courses of cervical medial branches across the articular pillars of the vertebrae. (From Lord SM, Barnsley L, Bogduk N: ­Neurosurgery Quarterly 1998;8:288-308, with permission.)

Figure 36-14  The target point for a cervical medial branch block at the centroid of the articular pillar of the vertebra where the cervical medial branch runs across it. (From Barnsley L, Bogduk N: Medial branch blocks are specific for the diagnosis of cervical zygapophysial joint pain. Regional ­Anesthesia 1993;18:343-350, with permission.)

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The suite should also be equipped for resuscitation and supportive care in the rare event of a serious complication arising. The test facility also requires a room where the patient can be prepared before the procedure and observed after the test has been performed. Equipment required in that part of the facility includes a device for measuring pain and charts on which pain scores can be recorded. The procedure begins with the preoperative phase. When a patient arrives at the test facility, he or she is admitted by a nurse who is trained in pain assessment. The nurse answers any questions the patient may have, checks for any contraindications such as allergy, infection, anticoagulant therapy, or pregnancy, and makes sure the patient has given informed consent (as described in the earlier section “Indications for Interventions”). After that, the nurse asks the patient to describe the pain for which the test is to be done; that pain is designated the “index pain.” For example, if a patient has headache and lower neck pain, the lower neck pain may be identified as the index pain for that day’s test. The nurse asks the patient about the intensity and distribution of the index pain, and those attributes are recorded on appropriate charts. The intensity is assessed by the patient as a score out of 10 or 100, using a printed visual analog scale (VAS) or some similar device such as a pain ruler, and recorded by the nurse on a pain chart. The distribution is recorded by the patient marking it on a body chart. The selection of the joint to be tested is checked by comparing the pain pattern drawn by the patient with the pain maps shown in Figure 36-7 to 36-11. The patient then changes into a hospital gown and at the appropriate time is taken to the procedure suite, preferably for the patient’s safety and convenience in a wheelchair. The operative phase begins when the patient reaches the procedure room. The patient is helped onto the x-ray table and positioned lying comfortably on their nonpainful side so that the painful side is uppermost (Fig.36-15). Their gown is tucked away from the neck and shoulder on that side. The skin of the area is sponged with a suitable antiseptic such as povidone-iodine or chlorhexidine and alcohol, allowed to dry and then draped with a sterile fenestrated drape. The operator, who should be wearing operating room scrubs, a surgical cap, operating mask and protective leads, should scrub their hands and don sterile gloves. The needles and other equipment for the procedure should be laid out on a sterile set-up (Fig. 36-16). Next the operator and the radiographer confer to ascertain the first target nerve. For example, if the patient is to have C5-6 MBBs, the first target nerve will be the C5 medial branch and its target point is at the centroid of the C5 articular pillar. When the first target is agreed, the radiographer obtains a clear lateral view of the target region and cones the image to it. Coning is important to minimize the exposure to the patient, the operator, and the radiographer to ionizing radiation. In the directly lateral view, the left and right articular pillars of the target vertebra will overlie each other and the target point will have a wide margin of bone around it, which enhances the safety of the procedure. Having obtained this view, the operator and the radiographer stand or sit so they can see the monitors clearly and carry out the procedure comfortably as in Figure 36-17. The MBB needling procedure should be performed in accordance with the protocol recommended by the International Spine Intervention Society (ISIS) and described fully in the relevant practice guidelines.140,141 It is important for the operator to talk to the patient to explain what is happening at each stage of the procedure, including what might be felt. The operator selects a suitable needle (usually a 25- or 26-gauge spinal needle at least 3.5 inches or 88 mm

Figure 36-15  The position in which a patient should lie on an x-ray table for a right cervical medial branch block.

Figure 36-16  A sterile set-up with skin preparation tray and equipment required for a cervical medial branch block. (Image courtesy of Pendlebury Clinic, Newcastle, Australia.)

in length) and with the plastic needle guard still on, places it on the skin of the patient’s neck to determine, by intermittent fluoroscopic images, the point on the patient’s skin directly over the target point; that will be the needle insertion site. Then the operator takes the guard off the needle, places its tip carefully on the patient’s skin at the insertion site and checks its position there with another intermittent image (Fig. 36-18). The operator stands the needle up in alignment with the fluoroscopic beam, warning the patient it will be felt, and inserts the needle through the skin as gently as possible. When the needle has purchase (i.e., when it has been inserted deeply enough to stand up

Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment  369

36

Figure 36-17  A fluoroscopy suite in which a patient is having a cervical medial branch block. Note the C-arm fluoroscope with image intensifier and high-resolution monitors. (Image courtesy of Pendlebury Clinic, Newcastle, Australia.)

Figure 36-19  Lateral fluoroscopic view of the right C5-6 zygapophysial joint with the needle tip on bone at the target point for a C5 medial branch block.

Figure 36-18  Lateral fluoroscopic view of the right C5-6 zygapophysial joint with the needle tip on skin over the centroid of the C5 articular pillar, the target point for a C5 medial branch block.

without being held) its position is checked on another lateral view. Then the operator guides the needle through the patient’s neck muscles toward the target point, steering it by moving its hub, shaft and/or bevel in ways that are learned in practical training. Before each adjustment of the needle its position is checked in an intermittent fluoroscopic view; continuous screening is avoided to keep the x-ray exposure to a minimum. When the needle tip reaches bone at the target point, its position there is checked and recorded on a fluoroscopic image, as in Figure 36-19. When the needle is in position with its tip at the target point, a syringe loaded with local anesthetic solution is connected to it by an extension tube and, after aspirating to check for blood, 0.5 mL of the local anesthetic is injected. The patient is then told the first of two blocks has been done and the same procedure will be followed to block the second nerve. The radiographer adjusts the fluoroscope to obtain a lateral view of

Figure 36-20  Lateral fluoroscopic view of the right C5-6 zygapophysial joint with the two needle tips on bone at the target points for C5 and C6 medial branch blocks.

the second target. The insertion point is determined and another needle is inserted in a similar manner, until its tip is resting on bone at the second target point. The position of the second needle at its target is checked and recorded on a fluoroscopic image, as in ­Figure  36-20, and 0.5 mL of local anesthetic is injected over the second medial branch. The patient is told both blocks are in place and the needles are about to be withdrawn, then that is done as smoothly as possible to complete the operative part of the MBB procedure. After the needles are out, the drape is removed and the antiseptic is sponged gently from the patient’s skin. Dressings are not

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usually required if 25- or 26-gauge needles have been used because they do not usually leave any mark, but if there is any bleeding small adhesive dressings may be applied. While still lying down, the patient is asked if they feel lightheaded or dizzy. If they do, they can be reassured that such symptoms are quite normal after a cervical nerve block and they should be allowed to lie quietly on the table until the dizziness settles, which may take a minute or two. When the patient is not dizzy, they are allowed to sit up with their legs over the side of the table, being supported by the operator and/or a nurse in case the change of posture makes them lightheaded. When they feel ready, the patient is helped from the table to a wheelchair and taken from the fluoroscopy suite to a room where they can rest and be observed by a nurse who is trained in pain assessment. The test procedure continues with the postoperative, observational phase. In the period after the injections a nurse who is trained in pain assessment asks the patient to score the intensity of the index pain at 30-minute intervals, beginning immediately after return to the observation area and continuing until 90 minutes later, and the resultant pain scores are recorded on a pain chart. When scoring the pain, the patient is advised to ignore any procedural pain from the needling and any pain they may have in other regions, and to focus on the index pain they scored before the block was done. To maximize the accuracy of the result, the procedure (and the observational phase in particular) should be undertaken to minimize potential biases that threaten the integrity of the process. These potential biases include reporting bias and observer bias. Reporting bias occurs if the patient describes their response to a block in ways that are influenced by misunderstanding of the purpose of the test or by their expectations or hopes, or if they wish (consciously or unconsciously) to please the recording nurse or the treating physician. Reporting bias may also occur if the patient is asked to describe their response some time after the test, such as the next day, when their memory of the postblock pain levels is less clear: this is termed recall bias.

PAIN CHART

Observer bias occurs if the recording nurse-observer is influenced by knowing when a patient’s pain might be expected to be relieved and when it might be expected to return. It may also occur if the nurse-observer wishes (consciously or unconsciously) for the patient to have a particular response to the block. These potential threats are minimized if the procedure includes a double-blind protocol for selection of local anesthetic agents, if the patient and the nurse-observer have clear ideas about the test process and the potential biases it may involve, and the postblock pain scores are recorded during what is called “real-time assessment.” A double-blind protocol for selection of local anesthetics means the agent to be injected on any occasion is allocated randomly by the operator. Neither the patient nor the recording nurse are aware of the agent used, so they cannot predict when the pain might be expected to be relieved and when it might be expected to return. A double-blind protocol controls the procedure for reporting and observer biases. If the patient and the nurse-observer are clear about the index pain, and postblock scores refer to it only and do not include any pain the patient may have elsewhere, the method is controlled for other potential reporting and observer biases. Realtime assessment (meaning the postblock pain scores are recorded at the actual times they occur) controls the process for recall bias. During the observational phase, the treating physician should stay away from the patient to avoid any interaction that might influence their responses. At the end of the observation period, the pain chart may be reviewed to determine the result of the test (Fig. 36-21). Cervical Medial Branch Block—Interpretation of Results Accurate interpretation of test results depends on understanding and applying the standards set out in the literature and specified in the relevant practice guidelines.140,141 A single MBB test result is deemed positive only if the index pain is relieved completely (i.e., its VAS score goes down to zero) in the postblock period, as shown on

(Score the index pain only and ignore any other pain) 100 90 80 70

X 76

60 V.A.S

50 40 30 20

X 14

10 0 TIME

X

X

X

Pre

Post

30 min

1 hour

90 min

1120

1205

1235

1305

1335

2 hrs

12 hrs

24 hrs

Figure 36-21  Pain chart showing the initial intensity of the index pain and the visual analog scale (VAS) scores recorded after a medial branch block test that produced an analgesic response. (Courtesy of Pendlebury Clinic, Newcastle, Australia.)

Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment  371

the pain chart in Figure 36-21. Any other result showing the index pain was still present, even if at a reduced level of intensity, must be considered negative or inconclusive. A treating physician may be tempted to try to interpret a reduced pain score, say if a patient’s index pain is reduced from 86/100 to 14/100, but rational interpretation of such a result will be confounded by the possibilities. The reduced score may be because the joint tested is contributing to, but not wholly responsible for, the pain or because the pain is actually stemming from an adjacent joint and one of its medial branches was blocked in the test, or because of some bias in recording. Another factor to be taken into account in interpreting MBB responses is the possibility of false-positive and false-negative results. A study of cervical MBBs showed 27% of responses to single blocks are false-positive and 5% of responses are false-negative.142 That means even if the index pain is relieved completely after an MBB, the pain is only 73% likely to be stemming from the joint blocked and if the index pain is not relieved after an MBB, the pain is only 95% likely to be not from that joint. The same study considered the positive predictive values (PPVs) of positive single block responses. PPVs vary with the prevalence of the condition; if the prevalence is as high as 70%, the PPV of a positive block response is only 89%. The liabilities of false-positive single block results are overcome by performing comparative blocks.143 If a patient has a positive response to an MBB, a second block is performed on a separate occasion to test whether the first result was true-positive. The second block is done following the same procedure but using another local anesthetic agent with a different duration of action. If the patient again has complete relief of the index pain after the second block, the durations of the responses can be compared. If the duration of pain relief was longer with the longer acting anesthetic (bupivacaine) than with the shorter acting (lidocaine), that joint is positively identified as the source of the index pain and the result is described as “comparative block positive and concordant,” which is the criterion standard for definitive diagnosis of cervical ZJ pain.140,141 Any other combination of results makes a comparative block test negative or inconclusive. C7 Medial Branch Block—Procedure Blockade of the C7 medial branch involves a slightly different technique because the nerve runs over a different part of its vertebra and has a wider range of anatomic variation in its course (see Fig. 36-12).139 It usually passes forward over the bony surface of the tip of the superior articular process of the C7 vertebra, somewhere between its peak and the root of the transverse process, but in some individuals it is superficial to the bone rather than immediately adjacent to it because the nerve is separated from the bone by a slip of the semispinalis capitis muscle. To ensure blockade of the nerve, wherever it happens to lie, requires injections of 0.3 mL of local anesthetic at each of two target points, one on the lateral aspect of the curved surface of the articular process up near its peak and the other 4 mm superficial to that. The first part of the procedure is similar to that followed at other cervical levels. When the needle tip reaches bone on the C7 vertebra at the initial target site, its position is checked (first) in a lateral view (Fig. 36-22). The C-arm is then rotated 90 degrees for a direct AP view. In that view, the needle position is checked again to ensure its tip is on the “skyline,” (i.e., on the lateral edge of the articular process, not around on the anterior or posterior parts of the bone’s curved surface) and that the tip is above the transverse process (Fig. 36-23). If the needle tip is in the correct position, the first injection of 0.3 mL of local anesthetic is done while the needle tip is on bone.

The needle is then withdrawn 4 mm and the position of its tip is recorded again off bone in an AP view before the second injection is made. The rest of the procedure is as described for the C3-4 to C5-6 levels. Third Occipital Nerve Block—Procedure The C2-3 ZJ is supplied by a single nerve, the third occipital nerve (TON) on that side which is the medial branch of the dorsal ramus of the C3 spinal nerve. Accordingly, the test procedure at the C2-3 level

Figure 36-22  Lateral fluoroscopic view of the right C6-7 zygapophysial joint with the needle tips on bone over the centroid of the C6 articular pillar and the peak of the C7 articular pillar, the target points for C6 and C7 medial branch blocks, respectively.

Figure 36-23  Anteroposterior (AP) fluoroscopic view of the right C6-7 ­zygapophysial joint with the needle tips on bone at the target points for   C6 and C7 medial branch blocks.

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that corresponds to MBBs at lower cervical levels is called a third occipital nerve block (TONB). The TON is thicker than other medial branches and that must be taken into account in consideration of procedures directed at it. Also, the TON carries some sensory fibers from a small patch of skin over the occipital region behind the ear on that side. Other medial branches generally do not carry skin sensation and this makes a difference to the observations after a TONB. The general course of the TON is forward over the C2-3 ZJ in the pericapsular fascia to join its dorsal ramus in the C2-3 intervertebral foramen. The course varies between individuals so the nerve passes somewhat horizontally across the joint at a level that ranges between the top and just below the bottom of the intervertebral foramen (see Figure 36-12).139 To ensure blockade of the TON wherever it happens to lie in this range requires injections of 0.3 mL of local anesthetic at each of three target points, which lie in a vertical line over the middle of the joint—a high one at the level of the apex of the C3 superior articular process; a low one at the level of the bottom of the C2-3 intervertebral foramen; and a middle one halfway between the other two (Fig. 36-24). In other respects, the procedure is similar to that used for cervical MBBs at lower levels, although in the operative phase, only one needle is inserted and it is moved to each of the target points in turn. The patient is positioned on the x-ray table lying on his/her side with the painful side up. The insertion site is determined by the needle being placed on the skin of the patient’s neck over the middle target point (Fig. 36-25). The operator inserts the needle and steers it to each of the three target points in turn. At each target, the needle tip position is checked and recorded on a lateral fluoroscopic image (Figs. 36-26-36-28) and 0.3 mL of local anesthetic is injected. After the patient is taken from the fluoroscopic suite and their postblock responses are being recorded, there is an extra observation to be made in the case of a TONB. The observer should ask the patient if any numbness is felt. If an effective TONB has been achieved, the patient will usually have numbness of the small area of skin behind the ear on the side that the TON supplies; a lack of numbness suggests the block may not be effective. As with other MBBs, if a single test relieves the index pain completely, a second comparative block should be done to determine if the first result is true-positive.

the test assesses what it is intended to assess. There are three domains of validity: face validity, construct validity, and predictive validity—all of which contribute to the overall validity of any ­diagnostic instrument. Face validity refers to whether a test or instrument appears, on the face of it, to assess what it is meant to assess. Cervical MBBs depend on the effects of blocking specific target nerves (and no others). Their face validity depends on whether they appear to block the target nerves only, (i.e., on their target-specificity). A study of the target-specificity of cervical MBBs137 showed that when the blocks are performed in the manner described, in accordance with

Figure 36-25  Lateral fluoroscopic view of the right C2-3 zygapophysial joint with the needle tip on skin over the target area for a third occipital nerve block.

Cervical Medial Branch Blocks—Validity Validity, in the biologic sciences, is concerned with legitimate interpretation of observed phenomena. The validity of a diagnostic test, like comparative MBBs, is the extent to which

Figure 36-24  The three target points for a third occipital nerve block(arrows). (From Barnsley L, Bogduk N: Medial branch blocks are specific for the diagnosis of cervical zygapophysial joint pain. Reg Anesth 1993;18:343-350, with permission.)

Figure 36-26  Lateral fluoroscopic view of the right C2-3 zygapophyseal joint with the needle tip on bone at the high target point for a third occipital nerve block.

Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment  373

the standard guidelines and injecting the volumes specified, the injectates will cover the target nerves but will not spread to any other nerves. Therefore, cervical MBBs have face validity. Construct validity refers to whether the interpretation of a measurement or test result reflects the theoretical construct of the

Figure 36-27  Lateral fluoroscopic view of the right C2-3 zygapophysial joint with the needle tip at the middle target point for a third occipital nerve block.

Figure 36-28  Lateral fluoroscopic view of the right C2-3 zygapophysial joint with the needle tip on bone at the low target point for a third occipital nerve block.

phenomenon to be observed. The theoretical construct on which cervical MBBs depend is that a cervical ZJ generating pain can be identified by blocking the nerve(s) along which pain is transmitted from the joint. The construct validity of cervical MBBs depends on the extent to which positive or negative block results reflect that the joint tested is, or is not, a pain source. The sections on interpretation of results makes it clear that single cervical MBBs do not, on their own, identify painful joints definitively but double-blind controlled, comparative cervical MBBs, with positive and concordant results, do have construct validity. Predictive validity refers to whether an instrument such as a diagnostic test is of value in predicting responses to treatment. It is directly related to therapeutic utility and of the greatest significance in the clinical application of diagnostic procedures like MBBs. The predictive validity of cervical MBBs depends on whether their results predict the likelihood of treatment being effective for relieving conditions diagnosed by the test. Positive and concordant, comparative MBB or TONB results identify pain stemming from a specific cervical ZJ on the basis of that pain being transmitted via the medial branch(es) blocked in the test procedure. Percutaneous radiofrequency cervical medial branch neurotomy is a therapeutic procedure established as effective for the treatment of cervical pain mediated via specific medial branches by the data of studies139,144,145 that used positive and concordant, comparative MBB, or TONB results as the indications for the treatment procedure. Hence, comparative cervical MBBs and TONBs, performed in those studies as described, have predictive validity. Because they have face validity, construct validity, and predictive validity all based on sound, published data, cervical medial branch blockade is described in the ISIS practice guidelines141 as an established procedure. There are many other publications on cervical blocks that touch on aspects of validity, including papers on procedures that sound like MBBs but are done in ways that differ from the standard guidelines, and the data from all those publications are extensive. Authors have described using placebo injections as an additional arm of a comparative block protocol146; studies of the efficacy of cervical radiofrequency neurotomy139,144,145 show that the results of comparative cervical MBBs using two local anesthetics and those of placebo-controlled comparative blocks have the same predictive validity for the outcomes of medial branch neurotomy treatment. Other authors have described MBB procedures that include the injection of contrast medium to confirm injectate spread147 but their results do not contradict those of the earlier study137 showing the target-specificity of MBBs done as described earlier. Placebo controls and contrast injection may be of value in specific circumstances, such as in research or for medicolegal purposes, but MBB and TONB procedures as laid down in the standard guidelines140,141 (and as described in this chapter) are of known, established validity for use in regular clinical practice. The data on validity in the foundation literature, on which the guidelines are based, are applicable to MBBs and TONBs performed as described. Those data cannot be generalized to blocks done in other ways, so such blocks cannot be assumed to be valid on that basis. In the absence of specific scientific evidence, whether blocks that are not performed in accordance with the standard guidelines are valid or not is simply unknown. Confusion about this has given rise to controversies about the reliability and validity of diagnostic block procedures in general; such controversies would diminish if block procedures were evaluated on the basis of the specific scientific evidence that applies to them.

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Thoracic Medial Branch Blocks—Procedure The thoracic medial branches run forward from above and below the thoracic ZJs they supply and over the transverse processes of the joint partners to join their respective dorsal rami in the intervertebral foramina. The numbering of the thoracic medial branches is one less than the vertebrae over which they run as explained in the earlier under “Anatomy”. This numeric variation need not be confusing if its pattern is appreciated. The T3-4 ZJ is supplied by the T2 and T3 medial branches, which run over the T3 and T4 transverse processes, respectively. The procedure to test the T3-4 ZJ as a source of pain involves blocking each of those two nerves. Even if they appreciate the numeric relationships between nerves and joints, it is important for clinicians to realize the potential for confusion and to be consistent in describing any procedure by the joint, or nerves, involved. The ISIS convention for designating joints by the use of a hyphen16 (e.g., the left T7-8 ZJ), is recommended for all written records. The courses of the thoracic medial branches have been plotted by cadaveric dissection studies.148 The upper and lower thoracic medial branches are reliably found on the bony surfaces of the thoracic transverse processes but the midthoracic medial branches are usually suspended in the soft tissues of the intertransverse spaces, as shown in Figure 36-29. These thoracic medial branches are accessible for injection around them as they pass over the transverse processes. The target points are, generally, near the superolateral corners of the transverse processes, on the backs of the costotransverse joints. A needle can be placed onto the target point for a thoracic MBB most readily from a posterior approach. The facilities and equipment required are the same as specified for cervical MBBs. A thoracic MBB procedure should be performed in accordance with the protocol described in the relevant practice guidelines.140,149 The needling part of the procedure must be undertaken with particular care because thoracic needling carries the risk of pleural puncture and pneumothorax. To minimize that risk, the guidelines must be followed meticulously. The procedure involves three phases similar to those described for cervical MBBs. The patient is positioned lying prone on the x-ray table and the skin of the thoracic region is swabbed and draped. The operator and the radiographer confer to ascertain the level to be tested and the first target nerve. For instance, if the patient is to have medial branch blocks to test the T3-4 ZJ, the first target nerve will be the T2 medial branch and its target point is near the superolateral corner of the T3 transverse process, on the back of the T3 costotransverse joint. When the first target is agreed, the radiographer obtains an AP view of the region. On that view, both operator and radiographer should count down the ribs from above to confirm the target level. When they agree, the radiographer cones the image to the region of the target joint and the adjacent transverse processes on that side. In the directly AP view, the ZJ itself will not be seen but its position can be inferred as being between the adjacent pedicles and immediately posterior to the corresponding intervertebral foramen. The transverse processes will be seen with the ribs in front of them, the top of each rib projecting above the top of the corresponding transverse process. The target point for each of the T1 to T4 medial branches is on the dorsal surface of the transverse process, below its upper border near the lateral end, so not quite the superolateral corner of the transverse process but slightly medial to it. The target point for each of the medial branches from T5 to T8 is not actually on bone but just above the superolateral corner of the transverse process

T1 T2 T3

T7 T8 T9

T4

T10

T5

T11

T6

T12

T7

L1

Figure 36-29  Plots of the courses of thoracic medial branches across the transverse processes of the vertebrae. (From Chua WH: Clinical Anatomy of the Thoracic Dorsal Rami [thesis]. Newcastle, Australia, University of ­Newcastle, 1994, with permission.)

and behind the dorsal surface of the rib that articulates with the transverse process. The target points for the T9 and T10 medial branches are like those for the T1 to T4 nerves, on the outer parts of the transverse processes. The target point for each of the T11 and T12 medial branches is at the junction of the root of the superior articular process and the root of the transverse process; this is best seen in an oblique “Scottie dog” view. In that view the target vertebra resembles a Scottish terrier, the superior articular process making the dog’s ear, the transverse process and pedicle making its head, the pars articularis its neck and the rest of the posterior elements making the dog’s body. Having obtained a suitable view, the operator selects a suitable needle, determines the insertion point, inserts the needle, and directs it to the target site as described for cervical MBBs. It is important to keep the needle tip over the bone of the transverse process at all times, to avoid the danger of pleural puncture. Before each adjustment of the needle, its path toward the target point should be checked on intermittent AP views, and the depth of insertion should be checked on intermittent lateral views. When the needle tip reaches bone at the target point, or the point just above the transverse process and behind the rib for T5 to T8 medial branches, its position is checked and recorded first in a lateral view and then in an AP view (Fig. 36-30). The first injection, of 0.5 mL of local anesthetic, is made at that site. Then the second target point is injected similarly. Thoracic Medial Branch Blocks—Interpretation of Results As with cervical MBBs, a single thoracic MBB test result is positive only if the index pain is relieved completely (i.e., its VAS score goes down to zero) in the postblock period. Any other result, with postblock index pain scores of more than zero must be considered negative or inconclusive. If the first block is positive, the issue arises as to whether it is true-positive or false-positive. This is even more important than it is for cervical blocks, because a study has shown single thoracic MBBs have a false-positive rate of 58%.64 Comparative blocks must be done before any sensible conclusion can be drawn from thoracic MBB results. Only two comparative block results that are both positive and concordant can be interpreted as identifying a specific thoracic ZJ as a pain generator.

Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment  375

36 TP mal SP

IC

Figure 36-30  Anteroposterior (AP) fluoroscopic view of a needle at the target point for a thoracic medial branch block. Contrast medium (0.5 mL) has been injected to show the spread of injectate.

Thoracic Medial Branch Blocks—Validity Rational consideration of the validity of thoracic MBBs is problematic because there are no data on which a justifiable evaluation can be based. For this reason, the ISIS practice guidelines describe thoracic medial branch blockade as an “emerging” rather than an “established” procedure. Thoracic MBBs may have face validity on the grounds that they appear prima facie to test what they are meant to test but there are no data to support this. There are no published studies of the targetspecificity of thoracic MBBs and no legitimate assumption can be made on the grounds of target-specificity of MBBs in other spinal regions. The variable courses of thoracic medial branches, and particularly the fact that the midthoracic medial branches do not lie on bone but are suspended in the intertransverse spaces where they are hard to locate, weigh against the face validity of thoracic MBBs. In the absence of sound data on target specificity, thoracic MBBs cannot be said to have face validity. The construct validity of thoracic MBBs would depend on the extent to which positive or negative block results reflect that the thoracic ZJ tested is, or is not, a pain source. Again, there are no sound data on which to base a rational evaluation but the high falsepositive rate of thoracic MBBs militates against their construct validity. Even if thoracic MBBs did have verifiable face and construct validity, they cannot be said to have predictive validity because there is no specific treatment proven effective, on the basis of published data, for the treatment of thoracic ZJ pain. Thus, no legitimate conclusion can be drawn about whether thoracic MBBs predict the likelihood of treatment being effective. Lumbar Medial Branch Blocks—Procedure Lumbar medial branch blockade is an established diagnostic procedure. It involves blocking the nerves that transmit nociceptive signals from lumbar ZJs so as to determine whether a specific ZJ is a pain generator. Each lumbar ZJ has sensory innervation via two nerves. The joints from L1-2 to L4-5 are each supplied by articular fibers of two medial branches, numbered like the thoracic medial branches and for the same reason, as one less than the joint they supply. Thus, the L4-5 ZJ has sensory innervation via the L3 and

Figure 36-31  Oblique diagram of the L3 and L4 medial branches, and the L5 dorsal ramus, running across the bases of the superior articular processes and accessible for injection at the points marked by arrows (the “eyes of the Scottie dogs” as seen in oblique fluoroscopic views).

L4 medial branches. The L5-S1 ZJ has its innervation by articular fibers of the L4 medial branch above it and articular fibers that go directly to the L5 dorsal ramus below. The L1 to L4 medial branches receive articular fibers from the tops and bottoms of adjacent ZJs and run through the mamillo-accessory notches, under the mamillo-accessory ligaments, and then across the bases of the superior articular processes near where they join the transverse processes. The numbering is such that the L1 medial branch runs across the superior articular process of the L2 vertebra near where it joins the L2 transverse process. The L5 dorsal ramus runs across the superior articular process of the S1 sacral segment near where it joins the ala of the sacrum (which is analogous to a transverse process). These nerves are accessible for blocking because they run across the bases of the superior articular processes, at the points marked by arrows in Figure 36-31. These points each correspond to the “eye” of a Scottie dog configuration as seen in an oblique fluoroscopic view. If the variation of joint and nerve numbering seems confusing, it may help to remember that the target points for a lumbar ZJ are near the roots of the transverse processes of the same designation (i.e., the target points for MBBs of the L4-5 ZJ are near the roots of the L4 and L5 transverse processes). As with thoracic structures, to avoid ambiguity when referring to a procedure targeting lumbar ZJs and medial branches, it is important to describe it by the joint or the nerves involved, explicitly. The lumbar MBB procedure, like those of cervical and thoracic MBBs, involves a preoperative phase, an operative (needling) phase, and a postoperative (observational) phase, and when results are at hand, their interpretation which may be considered a fourth phase. The phases are much the same as those described for the other spinal regions. To ensure validity, the procedure should be carried out in accordance with the standard guidelines.140,150 The patient is positioned lying prone on the x-ray table and the skin of their lumbar region is exposed, swabbed, and draped. The operator and radiographer ascertain the spinal level to be tested and the radiographer obtains an AP view of the region. On that view, both operator and radiographer should count down the lumbar vertebrae from the last thoracic vertebra that has a rib attached. If there seem to be six lumbar vertebrae because the first sacral

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considered in conjunction with the relatively low prevalence of lumbar ZJ pain, the high false-positive rate renders the positive predictive value of a single test unacceptably low.152 To compensate for these liabilities, controlled, comparative blocks must be performed, as in other spinal regions, before valid conclusions can be drawn. For maximal diagnostic confidence based on lumbar MBB results, because of the high false-positive rate and the low prevalence, these comparative blocks must include placebo controls.154 Placebo injections must only be given with informed consent but that is usually obtained readily if patients are told about the value of the extra control to the interpretation of the test results. Two comparative MBB results that are both positive and concordant, and a negative placebo control result, can be interpreted as identifying a specific lumbar ZJ as a pain generator.

Figure 36-32  Oblique “Scottie dog” view of the right L4-5 zygapophysial joint with needle tips on bone at the target points for blocking the L3 and L4 medial branches. From the lower needle, contrast is seen flowing into a regional vein (black arrows).

segment is lumbarized, or if any other anatomic variation is noted, the joint to be tested should be confirmed. When the target level is agreed, the radiographer swings the C-arm along the patient to focus on the end-plates of the vertebrae of that segment in an AP view, and then moves it across to obtain an ipsilateral oblique (Scottie dog) view of the target region and cones to it. The target point will be the “dog’s eye.” To block each nerve the operator takes a suitable needle, determines the insertion point, inserts the needle and directs it to the target site as described for cervical MBBs. It is important to keep the needle tip over bone at all times to avoid overshooting the target. Before each adjustment of the needle, its path toward the target point should be checked on intermittent oblique views. When the needle tip reaches bone at the target point, its position is checked and recorded in an oblique view (Fig. 36-32). Prior to the injection of local anesthetic, 0.5 mL of nonionic contrast medium should be injected to test for intravascular placement. This is done because a study has shown that at the target points for lumbar MBBs, the needle tip is intravascular in 8% of cases151 and if so, any injectate would be carried away in the blood and produce a false-negative result. If the contrast shows the needle tip is not intravascular, 0.5 mL of local anesthetic is injected. Lumbar Medial Branch Blocks—Interpretation of Results As with other medial branch blocks, a single lumbar MBB test result is positive only if the index pain is relieved completely. Any other result must be considered negative or inconclusive. If the first block is positive, the question arises as to whether that is a true-positive or false-positive result. One study showed that single lumbar MBBs have a false-positive rate of 38%152; other studies have shown false-positive rates between 25% and 41%.74,153 The practical effect of those rates is that if the true-positive to false-positive ratio is simplified conservatively as 2:1, of every three positive lumbar MBB results only two will be truly positive. When

Lumbar Medial Branch Blocks—Validity The face validity of lumbar MBBs depends on whether they appear prima facie to test what they are meant to test. Evidence of their face validity is provided by a study of the target-specificity of lumbar MBBs which showed that 0.5 mL injectates at lumbar MBB target sites cover the medial branches and do not spread to any other diagnostically significant structures.151 The construct validity of lumbar MBBs depends on the extent to which positive or negative block results reflect that a lumbar ZJ tested by them is, or is not, a pain source. A randomized, controlled trial showed lumbar MBBs anesthetize painful lumbar ZJs in 89% of cases.155 The issue of false-positive results is addressed by performing placebo-controlled, comparative blocks, as described earlier. False-negative results of lumbar MBBs have been shown to occur at a rate of 8% due to intravascular injection151 but that issue is addressed by preinjection of contrast medium. When performed as described, with contrast injection to check for intravascular needle placement and in comparative series with placebo controls, lumbar MBBs do have construct validity. The most practical domain of validity is predictive validity or therapeutic utility. Lumbar MBBs have been shown to have predictive validity by studies of percutaneous radiofrequency lumbar medial branch neurotomy. These studies show that therapeutic procedure is effective for the relief of lumbar ZJ pain when it is performed on the basis of positive and concordant, controlled, comparative, lumbar MBBs.156,157

Diagnostic Intraarticular Blocks Development Intraarticular blocks (IABs) of ZJs were developed long before MBBs and for some years were used as diagnostic tests for ZJ pain. In the light of the current scientific literature, IABs of ZJs must now be considered obsolete for diagnostic purposes. Medial branch blocks are much more appropriate as diagnostic tests because they are easier to perform, less invasive, safer and validated by the comparative block protocol set out in the standard guidelines. By contrast, IABs of ZJs are more difficult to perform, especially when the joint space is narrowed or occluded by osteophytes. MBBs involve needling of skin, subcutaneous tissues, muscles, and periosteum only, whereas IABs involve intrusion into the joint where the needle may damage delicate intraarticular structures. In MBB procedures, the needle tip can be kept over bone, which prevents inadvertent intrusion into nontarget structures but when IABs of ZJs are done, it is possible for the needle to pass right through the joint and into the adjacent spinal canal, where it may damage the spinal cord or nerve

Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment  377

roots. When comparative MBBs are performed in accordance with the standard guidelines they are of proven validity, whereas there are no data on the validity of ZJ IABs. Even if comparative IABs were performed, the differential effects of anesthetic agents inside joints are not known. For these reasons diagnostic IABs of ZJs are not recommended and they will not be described in this chapter. The lateral atlantoaxial (C1-2) and atlantooccipital (C0-1) joints have nerve supplies quite different from those of the ZJs, as described under “Anatomy”. The lateral atlantoaxial (C1-2) and atlantooccipital (C0-1) joints are supplied via the ventral rami of their respective spinal nerves, not via the medial branches and dorsal rami as are the ZJs. Thus, the procedures of MBBs have no application for the joints of the C0-1 and C1-2 spinal motion segments. Diagnostic blocks of the ventral rami are not practical because of the other structures those nerves supply. Therefore, the lateral atlantoaxial (C1-2) and atlantooccipital (C0-1) joints are tested as sources of pain by intraarticular blockade. Diagnostic IABs of the LAAJs were first described in 1987.158 LAAJ blocks are described in the ISIS practice guidelines as an established procedure159 and will be described here. Diagnostic IABs of the atlantooccipital joints are not described at all in the guidelines, not even as an emerging procedure, because they are not supported by evidence of safety and validity; accordingly, they will be addressed only briefly in this chapter. Lateral Atlantoaxial (C1-2) Joint Blocks—Procedure The LAAJs have been shown to be injured in traumatic events62 and are reported as sources of cervicogenic headache94,95,160 in the distribution illustrated in Figure 36-8. LAAJ blocks should be considered in the diagnosis of a patient with headache in that distribution and a history that suggests the possibility of LAAJ injury. Headache in that distribution may also stem from the C2-3 and C3-4 ZJs, and cervicogenic headache is believed to be more commonly associated with those upper ZJs, so it is prudent to test the C2-3 and C3-4 ZJs first. The main indication for diagnostic LAAJ blocks is for the investigation of cervicogenic headache when C2-3 and C3-4 blocks have proved negative, or when there is residual cervicogenic headache after C2-3 and/or C3-4 headache has been treated effectively. Intraarticular blocks of the LAAJs are performed via a posterior approach. As for any invasive procedure, it is vital for the operator to have sound knowledge of the regional anatomy. In relation to an LAAJ block, the operator must be aware of two important anatomic structures, the vertebral artery and the C2 dorsal ramus, which lie very close to the target joint. The vertebral artery is usually located immediately lateral to the LAAJ but within the normal range of anatomic variation it may be posterior to the lateral part of the LAAJ. The dorsal ramus of the C2 spinal nerve passes superomedially across the back of the superior articular process of the axis (i.e., just behind the lower process of the LAAJ). To avoid inadvertent puncture of either of those structures, the operator must be meticulous in following the guidelines for the procedure.159 The most appropriate local anesthetic for the block is 2% lidocaine. Longer-acting local anesthetics such as bupivacaine should not be used at the atlantoaxial level because if it should leak from the capsule, it could cause prolonged high spinal block. Each LAAJ block procedure involves a preoperative phase, an operative needling phase, and a postoperative observational phase, followed by the diagnostic interpretation of test results (much as described for cervical MBBs). In the operative phase, the patient is positioned lying prone on the table and made comfortable with the neck flexed; the neck is swabbed with antiseptic and

draped. Throughout the operative phase the patient should be kept informed of its progress because they are lying face down with their head covered and may feel vulnerable. The radiographer obtains an AP view of the patient’s upper neck and moves the C-arm longitudinally until the LAAJs are seen as ellipsoid structures on either side of the odontoid process near its base. Both the operator and the radiographer should identify the image of the arch of the axis, which can lie over the LAAJs in an AP view. If necessary, the radiographer angles the x-ray beam so the image of the arch of the atlas is well above the target joint and there is a clear view of the upper margin of the LAAJ in its middle third, which is the initial target point. The radiographer then cones to that area. The operator takes a spinal needle and locates the insertion site on skin over the target (Fig. 36-33). The needle is inserted and guided through the muscles as described for other blocks. Intermittent AP fluoroscopic views are used to keep the needle tip over the target zone and lateral views are used to check the depth of penetration (Fig. 36-34). When the needle tip reaches bone at the initial target point, on the upper margin of the LAAJ in the middle third of the inferior articular process of the atlas, its position is checked and recorded on AP and lateral fluoroscopic images (Figs. 36-35 and 36-36). The needle is then withdrawn slightly, directed downward and inserted into the joint. Another intermittent lateral view should be obtained to check the needle tip is intraarticular. A syringe of nonionic contrast medium is connected to the needle by an extension tube and the needle tip placement confirmed by injection of about 0.2 mL of contrast medium to produce an arthrogram of the LAAJ (Fig. 36-37). The C-arm is then rotated 90 degrees and the confirmatory arthrogram recorded on an AP view as well (Fig. 36-38). Taking care to keep the needle in place, the operator then draws back with the syringe to aspirate the joint and remove as much contrast medium as possible from it; if left there the contrast will occupy space to be taken by the local anesthetic. After that, another syringe and a fresh extension tube filled with 2% lidocaine is fitted to the needle, again taking care not to dislodge the tip, and about 0.5 mL or a little more of the local anesthetic is injected slowly, the operator being careful to feel the pressure as the joint cavity is infiltrated so as not to inject too large a volume and rupture the joint capsule. Then the needle is removed. Lateral Atlantoaxial (C1-2) Joint Blocks—Interpretation of Results As with other diagnostic blocks, a lateral atlantoaxial joint block is considered positive only if the index pain is relieved completely (i.e., its VAS score goes down to zero) in the postblock period. Any other result must be considered negative or inconclusive. If the first block is positive, the issue arises as to whether it is true-positive or false-positive. There are no sound data on the false-positive and false-negative rates of LAAJ blocks, but such possibilities can be envisaged. Comparative blocks cannot be done safely as for MBBs because it is not safe to inject long-acting local anesthetic at the atlantoaxial level of the spine, so if confirmation of a result is required, the best that might be done is to repeat the block on another occasion and compare the two results. Lateral Atlantoaxial (C1-2) Joint Blocks—Validity Lateral atlantoaxial joint blocks have face validity on the grounds of the confirmatory arthrograms recorded during the procedure. Those arthrograms show that LAAJ blocks are target specific. The construct validity of LAAJ blocks would depend on the extent to

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Figure 36-33  The anteroposterior (AP) fluoroscopic view required for an intraarticular block of the right lateral atlantoaxial joint. Note the image of the arch of the atlas, above and clear of the upper margin of the joint in its middle third (the initial target point) and the needle tip on skin over that point.

Figure 36-35  Anteroposterior (AP) fluoroscopic view of the right lateral atlantoaxial joint with the needle tip on bone at the initial target point for an intraarticular block.

Figure 36-34  Lateral fluoroscopic view of the right lateral atlantoaxial joint showing the needle passing under the arch of the atlas and on track toward the initial target point for an intraarticular block.

Figure 36-36  Lateral fluoroscopic view of the right lateral atlantoaxial joint with the needle tip on bone at the initial target point for an intraarticular block.

which positive or negative block results reflect that the joint tested by them is, or is not, a pain source. There are no numeric data on these aspects of LAAJ blocks. The predictive validity or therapeutic utility of LAAJ blocks is problematic because there is no simple, validated treatment for LAAJ pain. Intraarticular steroid injections are used by some but the evidence for their effectiveness is weak and based on practice audits95,161; there are no data from randomized, controlled trials. The only other treatment described is surgical fusion of the atlantoaxial segment162,163; although there is a place for such a procedure, there are no rigorous data to show that it is validly indicated by positive LAAJ blocks.

Atlantooccipital (C0-1) Joint Blocks The atlantooccipital (C0-1) joints have been reported to be pain sources94,161,164 and a pattern of cervicogenic headache associated with them has been described.94 Consideration of the morphology and biomechanics of the atlantooccipital (AO) articulations suggests that they are less likely to be injured, and so to give rise to articular pain, than other spinal joints. The most likely mechanism of injury would be distraction, as the AO joints have powerful restraints to other biomechanical threats. Be that as it may, the prevalence of AO joint pain is unknown. Diagnostic intraarticular blocks of the AO joints are possible in theory but are seldom performed in practice. It is certainly not a procedure to be undertaken

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Figure 36-38  Anteroposterior (AP) fluoroscopic view of a right lateral atlantoaxial arthrogram recorded to confirm correct placement of the needle tip for an intraarticular block. Figure 36-37  Lateral fluoroscopic view of a right lateral atlantoaxial arthrogram recorded to confirm correct placement of the needle tip for an intraarticular block.

because it can be. The technique of injecting an AO joint is a highly specialized one carrying significant risks of damage to vital structures including the vertebral artery, the internal jugular vein, and the vagus nerve, all of which lie adjacent to the joint. If an AO joint injection is considered necessary and the risks are worth taking, a lateral oblique approach is used with very careful control of the needle course on intermittent oblique fluoroscopic views and monitoring of the depth of insertion on open-mouth AP views. A posterior approach must not be used because the vertebral arteries cross the atlantooccipital joints posteriorly; any attempt to inject an AO joint from behind carries a serious risk of injuring the vertebral artery, with potentially disastrous consequences. Diagnostic AO joint blocks should not be attempted by anyone without rigorous practical training in the procedure. If needle position is confirmed by an arthrogram (Fig. 36-39) and a diagnostic block of the joint is achieved, the interpretation of the result is subject to the same liabilities as those of LAAJ joint blocks. The validity of diagnostic AO joint blocks is also limited like that of LAAJ blocks. If a confirmatory arthrogram is recorded, a block can be said to have face validity (target specificity). There are no data on the construct validity of AO joint blocks and very little data on their ­predictive validity or therapeutic utility—only two small data sets based on practice audits.161,164

Treatment of Zygapophysial Joint Pain Development ZJ pain can be diagnosed definitively, specifically and validly, by the careful application of medial branch block procedures. When it is, the question arises as to how to treat it. The treatment of pain of (or presumed to be of ) ZJ origin has a long and colorful history. An extensive range of treatments has been put forward over the years. Many of treatments are still done by a variety of practitioners to relieve pain thought to stem from ZJ impairment of some sort, and

Figure 36-39  Oblique fluoroscopic view of a right atlantooccipital (AO) arthrogram recorded to confirm correct placement of the needle tip for an intraarticular block. The four arrowheads mark the margins of the target AO joint, the thinner arrow indicates the top of the dens, and the thicker arrow indicates the lateral margin of the contralateral lateral atlantoaxial (LAA) joint.

variously believed to be due to injury, disease, mechanical dysfunction (including locking, displacement and/or hypermobility) and a host of other putative mechanisms. The forms of treatment still offered include physical modalities (heat, cold, infrared, ultrasound, laser, electrotherapy, massage, mobilization, manipulation), exercise programs, analgesic and anti-inflammatory medications, dry needling, “prolotherapy,” acupuncture, transcutaneous electrical nerve stimulation, other forms of neuromodulation such as spinal cord stimulation, spinal surgery (in particular arthrodesis), functional restoration, “back schools”, and psychological interventions such as cognitive behavioral therapy. These are only some of the “mainstream” treatments: the total range is vast and only limited by human imagination.

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All these treatments have their places in the broader scheme of things and are justified to various extents by types of supporting evidence ranging from anecdotal testimonies to rigorous scientific data. The purpose of this chapter is to describe particular interventions used in the management of ZJ pain by practitioners of pain medicine or spine care. Even in those fields, individual practitioners differ in their approaches. To avoid drifting into uncertain areas, this chapter has an anchor in reality in the form of the scientific evidence base; it is limited (in the main) to interventions supported by scientific data for the diagnosis and treatment of ZJ pain. Two types of treatment for ZJ pain, intraarticular injections of corticosteroid and percutaneous radiofrequency medial branch neurotomy, will be described and the evidence relating to them will be reviewed. Therapeutic Intraarticular Joint Blocks—Procedure Intraarticular injections of corticosteroid are a traditional form of treatment used by physiatrists, rheumatologists, and others in the management of peripheral joint pain. The concept has been applied to spinal joints and therapeutic intraarticular joint block procedures have been developed. These procedures, designated by some as “facet blocks,” are readily performed by those with sound knowledge of regional anatomy and practical skills in fluoroscopicallyguided injection techniques. A cervical ZJ is most easily injected via a lateral approach but the procedure must be performed cautiously, with intermittent lateral views to guide the needle path and careful control of the depth of penetration on intermittent AP views, to avoid the danger of the needle passing right through the joint and into the spinal cord. An upper or midthoracic ZJ is best injected via an approach from behind and below, so the needle tip enters the joint at the midpoint of its lower margin; the needle course must be controlled carefully with intermittent AP views to ensure the needle tip stays over bone and does not stray laterally, where it may cause inadvertent pleural puncture, or medially, where it may enter the intervertebral foramen. The lowest two thoracic ZJs, and the lumbar ZJs, are most easily injected from an oblique posterior approach controlled by intermittent oblique views of the Scottie dog projection. The procedure for each of these intraarticular injections involves three phases like those described for cervical MBBs. In the operative phase the patient lies on the table in the appropriate position (laterally, with the painful side up for cervical injections or prone for thoracic and lumbar procedures). All precautions for aseptic technique are followed, as described for MBBs. The operator and radiographer confirm the target joint and the radiographer obtains a suitable view and cones to the target area. The operator introduces the needle and the guides it through the muscles, taking care to check its path and depth of penetration on intermittent fluoroscopic views, until its tip reaches bone near the target joint. The position of the tip on the joint margin is confirmed on AP and lateral views. Then the tip is guided into the joint cavity. Its position intraarticularly is checked on further AP and lateral views and contrast is injected for a confirmatory arthrogram as described for diagnostic blocks of the LAAJs. Typical cervical, thoracic, and lumbar ZJ arthrograms are shown in Figures 36-40- 36-42. After the confirmatory arthrogram has been recorded, the operator aspirates and then injects the joint with a mixture of local anesthetic and a depot corticosteroid preparation. As with diagnostic intraarticular blocks, the operator must inject slowly and monitor the pressure of the injection to avoid rupture of the joint capsule. When about 1 mL of the mixture has been instilled, more or less depending on the pressure felt during injection, the needle

Figure 36-40  Lateral fluoroscopic view of a right C2-3 zygapophysial joint arthrogram recorded to confirm correct placement of the needle tip for a therapeutic intraarticular joint block.

Figure 36-41  Anteroposterior (AP) fluoroscopic view of a right T6-7 zygapophysial joint arthrogram recorded to confirm correct placement   of the needle tip for a therapeutic intraarticular joint block. Arrows indicate joint margins.

is withdrawn and the patient is taken from the fluoroscopy suite to rest and recover. Therapeutic Intraarticular Joint Blocks—Effectiveness Therapeutic intraarticular joint blocks have been used for the treatment of spinal joint pain for some years and remain in common use. The evidence of their effectiveness is not compelling. The reports of uncontrolled, observational studies,165-168 mainly of intraarticular corticosteroid injection of lumbar joints, gave the impression that

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branch neurotomy (MBN) is to change the chemical structure of the nerve fibers so they do not conduct nociceptive signals. Nerves treated by thermal RF undergo chemical change but their structure remains as before (like a hard-boiled egg). The maintenance of neural structure obviates the risk of neuroma formation, which occurred after neurectomy. To perform RF cervical MBN properly, making multiple heat lesions over the course of each target nerve from different directions, takes about an hour for each nerve treated, so a two-nerve procedure such as is necessary to treat each of the cervical ZJs (other than that at C2-3) takes about 2 hours. The equipment required for MBN includes, in addition to the facilities and equipment described for MBBs, an RF generator capable of producing a conventional, thermal RF field, a matched earth plate, connecting leads, and an RF electrode. A large-diameter (18 or 16 gauge) RF electrode should be used to avoid the inadequate effects that were reported in earlier times when smaller electrodes were used.177

Figure 36-42  Anteroposterior (AP) fluoroscopic view of a right L5-S1 zygapophysial joint arthrogram recorded to confirm correct placement of the needle tip for a therapeutic intraarticular joint block.

the treatment is effective for ZJ pain. These reports encouraged the use of corticosteroid injections for pain from spinal joints at all levels, including ZJs, LAAJs, and atlantooccipital joints. The results of randomized, controlled trials do not confirm the utility of the treatment. A randomized, controlled trial of cervical intraarticular corticosteroid injections for ZJ pain169 showed the treatment is not more effective than placebo. A randomized, controlled trial of lumbar intraarticular corticosteroid injections for ZJ pain170 also showed no benefit of steroid injections when compared to saline controls. There are no sound data from randomized, controlled trials for the effectiveness of intraarticular corticosteroid injections at other spinal levels. Radiofrequency Cervical Medial Branch Neurotomy—Development Radiofrequency medial branch neurotomy (RFMBN) is a treatment that evolved from earlier concepts of trying to relieve ZJ pain by interrupting conduction in the nerves that transmit nociceptive information from the joints. Early attempts at denervation of ZJs by injection of phenol,171 by cryotherapy172 and by surgical neurectomy173 either failed to achieve their purposes or had unacceptable unwanted effects, or both. In particular neurectomy, if it could be achieved, caused neuroma formation and deafferentation, both of which caused worse pain than that which the neurectomy was designed to relieve. In the 1970s, radiofrequency energy was explored as a means of treating nerves to prevent conduction of pain from ZJs.174 Success was claimed in descriptive studies of the technique but it was called into question when its stated targets were found to be inaccurate anatomically.175 Further research lead to the development of more useful techniques. In its evolution over the last 3 decades, RFMBN has appeared in several different forms. The most effective form, that set out in the ISIS practice guidelines176 and described in this chapter, involves placing an RF electrode parallel to, and closely up against, each medial branch nerve to be treated. Radiofrequency energy is then applied in such a way as to “cook” (i.e., coagulate by heat) a length of the nerve in the accessible part of its course. The purpose of medial

Radiofrequency Cervical Medial Branch Neurotomy—Procedure The percutaneous RF cervical MBN procedure involves three phases, a preoperative phase, an operative phase, and a postoperative, recovery phase. In the preoperative phase the patient is admitted to the treatment facility and checked by the admitting nurse in the same ways as described for diagnostic block procedures, but with extra attention to their understanding of the procedure planned and its effects. The nurse should make sure the patient understands that RFMBN is a much longer procedure than the diagnostic blocks they will have had previously, and they will need to lie still at certain stages. Any questions the patient may have should be answered by the nurse or referred to the treating physician, so the patient has all relevant information before giving informed consent in writing. The patient is then changed into a hospital gown for transfer to the fluoroscopy suite. For the operative phase the patient is positioned laterally on the x-ray table with the side to be treated up (see Fig. 36-15). They are made as comfortable as possible with padding under their lower shoulder and hip, and reassured that they will be kept informed of the progress of the procedure. Full aseptic precautions are observed to ensure a sterile field. The operator should scrub and put on a sterile gown and gloves, the image intensifier should be covered with a sterile cover, and the skin of the side and back of the patient’s neck should be swabbed widely with antiseptic and allowed to dry, then sterile drapes should be applied so the patient’s upper body is covered, except for the side and back of the neck, and the face. It is important to keep the face clear of drapes so the patient can see adequately, breathe easily, and communicate with the operator. The operator and the radiographer confer to confirm the nerves to be treated and the one to be treated first. Then the radiographer obtains a clear lateral view of the target joint and cones to it. The operative phase begins with an MBB of the first target nerve, done as described earlier for a cervical MBB. When the needle is on bone, the operator injects through it a long-acting local anesthetic such as bupivacaine 0.5%, in multiple small volumes up to about 1 mL in total to cover the articular pillar around the nerve. The needle should be left in situ with its tip on bone to mark the position of the target nerve. The C-arm is then swung though 90 degrees for an AP view in which the tip of the block needle is seen on the waist of the articular pillar of the target vertebra. A second spinal needle is inserted via a posterior approach so its tip meets that of the block needle. That second needle will lie along the path to be followed by the electrode

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Figure 36-43  Lateral fluoroscopic view showing an electrode in place on the articular pillar for percutaneous radiofrequency cervical medial branch neurotomy.

in its first (sagittal) pass. A short-acting local anesthetic, such as lidocaine 1%, is injected through the second needle as it is withdrawn slowly to anesthetize the electrode path. Then the electrode is introduced and directed along a sagittal course, with the guidance of intermittent AP and lateral views, until it rests on the articular pillar as shown in Figure 36-43. The position of the electrode is confirmed on an AP view to check it is lying snugly against bone, as in Figure 36-44. The first radiofrequency lesion is made at that site. The patient should be told the nerve is about to be “cooked” and they should lie still for the time it will take to make the lesion, but they must speak out to report any discomfort they feel during the lesioning process. The generator is then activated to heat the electrode tip to 85° C for 90 seconds. If the patient reports any pain while the energy is being applied, the RF generator should be switched off immediately, more local anesthetic injected via the block needle, and the electrode position readjusted if necessary and checked again before proceeding. After the first lesion is made and the electrode has cooled sufficiently, it is moved to parallel positions above and below the first position, and further lesions are made at those sites. Then the electrode is withdrawn. Another spinal needle is introduced for an oblique pass, at 30 degrees to the course of the sagittal one. In the oblique pass, the electrode will reach further forward on the articular pillar. Three more lesions are made there at 82° C. Six RF lesions are made over the target nerve so they overlap to make sure they cover the area where the nerve may lie. In some cases, when the articular pillar is taller than usual and the nerve may lie outside the field covered by the standard number of lesions, more than three lesions are required in each pass. After the first nerve has been treated adequately, the procedure is repeated to treat the other target medial branch and then the electrode is removed. The insertion sites are covered with sterile dressings and the surgical drapes are removed. When the operative phase is complete, the patient is transferred from the fluoroscopy suite for recovery. A cold pack is applied to the treatment site to minimize bruising. The patient should be warned to be careful because they may be unsteady while the local anesthetic is acting, told not to drive a vehicle that day, and advised to rest over the next few days. They should be provided with analgesic medication to relieve the soreness they will feel from the muscles

Figure 36-44  Anteroposterior (AP) fluoroscopic view showing an electrode in place snugly against the articular pillar for percutaneous radiofrequency cervical medial branch neurotomy.

through which the electrodes passed. When they feel ready, they can be allowed to go home. They should be followed up by telephone over the next few days until the postoperative soreness dissipates. Radiofrequency Cervical Medial Branch Neurotomy—Effectiveness The efficacy of RF cervical MBN has been demonstrated by the results of a rigorously designed, randomized, placebo-controlled clinical trial of the procedure done as described.144 The trial involved a relatively small number of subjects (N = 49) but the design of the study gave it immense statistical power (100%) which is far more important than the sample size. The method used in that trial was judged by objective assessors as the standard for the procedure178 and is the method described in the standard practice guidelines.176 Percutaneous RF cervical MBN, when validly indicated and performed in accordance with those guidelines using 18- or 16-gauge electrodes to make multiple overlapping lesions over the medial branches from sagittal and oblique passes, is an effective treatment for established cervical ZJ pain. Most patients will have complete relief of pain from the joint treated and of any disability caused by that pain.144,145 Any psychological distress associated with the pain can also be expected to resolve.179 If the patient has any residual neck pain after the postoperative discomfort has dissipated, it will be from another pain generator, possibly another injured ZJ that can be investigated and treated similarly. The effect of RF lesions made as described can be expected to last for an extended period. Data from studies with long followup show that after cervical MBN, total pain relief usually lasts for between 270 and 400 days (9 to 13 months).144,145,180,181 The treated nerves are coagulated but not destroyed anatomically and they will recover from the lesions over time. When they do, the pain will return but the RF treatment can then be repeated as needed to restore control of the pain and pain-related disability for as long as the problem persists. RF cervical MBN, when performed ­correctly and followed appropriately, can completely relieve patients of ­cervical ZJ pain. No other report has been published of a rigorously-designed, randomized, controlled trial of MBN for cervical ZJ pain, although

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there have been publications describing cervical RF procedures done in other ways. As with other spine interventions, it is strongly recommended that RF cervical MBN be undertaken in accordance with the standard method described in the standard guidelines, the method that has been proven effective. The establishment of a standard necessarily implies other methods are less acceptable. The data of the rigorous controlled trial of MBN144 cannot be generalized to “RF neurotomy” performed in other ways, such as procedures using smaller gauge electrodes, those aimed at different target sites and/or those in which fewer lesions are made over each nerve. Such procedures are likely to achieve less satisfactory outcomes. Systematic reviews that include reports of diverse procedures, all called “radiofrequency neurotomy” but done in different ways, will inevitably show a diversity of outcomes which can be perplexing for anyone trying to gauge the effectiveness of proper MBN treatment. Failure to appreciate the differences between procedures that are given similar names, but vary in fundamental ways, can lead to confusion and controversy. If so, the problem lies with the understanding, not with the standard method. This issue is addressed further under “Radiofrequency Lumbar Medial Branch Neurotomy—Effectiveness”. Radiofrequency Thoracic Medial Branch Neurotomy The principles of RFMBN could, in theory, be applied for treatment of thoracic ZJ pain. The targets would be the thoracic medial branches whose anatomic positions are described in the section “Thoracic Medial Branch Blocks”. The relationships of thoracic medial branches to other structures, especially the pleura, present technical difficulties in placing thermal RF lesions over the nerves safely. Some have undertaken thoracic RF procedures but those procedures must be considered experimental. No standard method has been described for RF thoracic MBN and there is no evidence of the effectiveness of any such procedure. Radiofrequency Lumbar Medial Branch Neurotomy—Procedure Percutaneous thermal RF lumbar MBN is an established procedure for the treatment of lumbar ZJ pain. It is performed in a way similar to that described for RF cervical MBN, using large-diameter (18 or 16 gauge) RF electrodes placed parallel to, and very close to, each of the medial branches that supply the target joint. The treatment should be undertaken in accordance with the protocol laid down in the standard practice guidelines182 for maximal safety and effectiveness. The RF lumbar MBN procedure involves three phases like those of the cervical treatment, a preoperative phase, an operative phase, and a postoperative, recovery phase. In the operative phase, the patient is positioned lying prone on the table and is made comfortable with suitable padding. Aseptic conditions are observed to ensure a sterile field. Local anesthesia is established and the block needle is left in place to mark the target zone. An RF electrode is introduced in an oblique direction from below and lateral to the target nerve, and aimed toward the target indicated by the block needle. The electrode is directed carefully through the muscles until its tip lies at the base of the superior articular process that the medial branch courses over, and on the posterior part of the adjacent transverse process, with the shaft of the electrode parallel to the nerve. The position and orientation of the active tip of the electrode is critical to the success of the procedure.183 When the electrode is in place at the target site, its position there is checked and recorded on AP, oblique and lateral views, as shown in Figures 36-45 and 36-46.

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Figure 36-45  Oblique fluoroscopic view showing an electrode in place at the junction of the superior articular process and transverse process for percutaneous radiofrequency lumbar medial branch neurotomy.

Figure 36-46  Lateral fluoroscopic view showing an electrode in place at the junction of the superior articular process and transverse process for percutaneous radiofrequency lumbar medial branch neurotomy.

With the electrode in the correct position, the patient should be advised that the nerve is about to be “cooked” and told to report any pain, feeling of heat or any other unusual sensation during the process. Then the generator is turned on to produce a thermal RF field that will coagulate the target nerve in a way similar to that described for cervical RF treatment. In the lumbar RF procedure only one pass of the electrode is required at each spinal level and two or three overlapping lesions over the course of each medial branch are enough to produce the desired therapeutic effect. Radiofrequency Lumbar Medial Branch Neurotomy—Effectiveness The therapeutic value of percutaneous RF lumbar MBN is controversial. The controversy, like that associated with cervical MBN, is related more to the diversity of RF procedures described in the

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literature than to the outcomes of valid lumbar MBN treatments. There are many more publications on lumbar RF procedures than on cervical ones, so the potential for confusion and controversy is much greater when lumbar treatments are being considered. When properly indicated (by positive, controlled, comparative MBBs) and performed in the manner described in the standard practice guidelines,182 percutaneous RF lumbar MBN is an effective treatment for chronic lumbar ZJ pain. In most cases, thermal RF treatment will relieve the pain from the target joint completely and free the patient of any disability related to that pain. If the patient has any residual ZJ pain after the procedure, it will be from another source that may be treated similarly. The published evidence of the effectiveness of thermal RF lumbar MBN is compelling but that is clear only when it is separated from the large amounts of data relating to other RF procedures. These may seem similar superficially but they are essentially dissimilar if they are done to treat different conditions, and/or are based on different indications, and/or involve different techniques, and/or are aimed at different targets. The potential for confusion is considerable. The effectiveness of RF lumbar MBN was demonstrated first by the report of a randomized, controlled clinical trial published in 1999,184 which showed substantial benefits of the RF procedure over placebo. Although the pain relief was significantly greater in the treatment group (showing that coagulating nerves is better than a sham treatment), the results of the trial are compromised by two factors. First, it included patients on the basis of 50% or more relief of pain after single MBBs (so the study population would have been mixed) and it used a technique in which the electrodes were placed perpendicular to the target nerves, not parallel to them (so only short lengths of nerve were likely to have been coagulated and, in many cases, the relief was only of brief duration). The trial data count as evidence of the effectiveness of medial branch coagulation but do not count as evidence for the full RF lumbar MBN procedure as described in the standard practice guidelines. Another controlled trial published in 2007,185 used a valid RF technique with electrodes placed parallel to the medial branches. It again showed that conventional, thermal RF coagulation is more effective than placebo, and also more effective than a “pulsed RF” technique which was also tested in the study. The inclusion criteria for this trial were clinical features and a single positive MBB only, so again the study population would have been mixed. The thermal RFMBN outcomes of this study were better and lasted longer than those of the earlier controlled trial. These data again show the effectiveness of medial branch coagulation but because of the inclusion criteria, they do not count as evidence for the full RF lumbar MBN procedure. A further randomized, controlled clinical trial of RF lumbar MBN published in 2008,157 used positive, comparative MBBs as the diagnostic criterion and employed the RF technique recommended in the standard guidelines. It showed clinically (and statistically) significant relief of pain and improvements in quality-of-life indicators after the active treatment. These data are evidence of the effectiveness of the RF lumbar MBN procedure done in accordance with the standard guidelines. Another controlled clinical trial of RF lumbar MBN published in 2009,186 used a valid, parallel electrode technique and produced further evidence of the effectiveness of the treatment but it used a combination of a positive MBB and a positive intraarticular block as the indication for the treatment, so in that respect it did not conform to the standard criteria. The data from these four randomized, controlled trials are reinforced by the results of two descriptive outcome studies156,187

of RF lumbar MBN using positive, comparative MBB results as the indication for the treatment and valid, parallel electrode techniques in the therapeutic procedure. Both these studies showed that RF lumbar MBN, when properly indicated and performed according to the standard guidelines, is an effective treatment for lumbar ZJ pain. These data are supported by the conclusions of two systematic reviews of the literature published in 2002188 and 2009,189 which both found evidence in favor of the effectiveness of the procedure. This clear evidence of the effectiveness of RF lumbar MBN is overshadowed by the reports of several other studies and “systematic reviews” (including one review190 within the framework of the Cochrane Collaboration) which seem to show that the weight of evidence is against the effectiveness of lumbar RF procedures. As intimated earlier, confusion about different types of RF treatment has lead to controversy. Both the confusion and the controversy are easily resolved by considering the different methods used in lumbar RF treatments with specific focus on their validity (i.e., whether those methods achieve what they are intended to achieve). In this regard, the significant elements of any lumbar RF procedure are (1) its target, (2) its indications and (3) how that target is treated. In evaluating the evidence of the effectiveness of RF lumbar MBN for the treatment of ZJ pain, it is important to consider all reports of the outcomes of procedures that (1) target the lumbar medial branches, (2) were indicated by positive, controlled, comparative MBBs and (3) used a valid technique involving multiple lesions made by thermal RF fields applied with 18 or 16 gauge electrodes correctly positioned parallel to the target nerves. The 2008 randomized, controlled trial157 and the two descriptive studies156,187 showing effective RF treatment met all those criteria. Significantly, there are no other published studies that meet those criteria and have unsatisfactory outcomes. Thus, the evidence of the effectiveness of RF lumbar MBN for the treatment of ZJ pain is incontrovertible. The evidence on the effectiveness of lumbar RF treatment provides a good example of how controversies about interventions arise and how they are resolved. From a scientific point of view, skepticism is always to be encouraged and any doubts raised should be dispelled by considering all relevant scientific evidence. That is the rationale of evidence-based medicine. Current principles of ­evidence-based medicine flowed from the ideas of Archie Cochrane,191 a Scottish physician who practiced from the 1930s until the 1980s. Cochrane advocated the evaluation of medical interventions by consideration of the scientific evidence of their outcomes. His ideas lead to development of the systematic review, a process in which all relevant, scientific evidence is collated and analyzed to produce a summary of current knowledge of the topic, on which rational management decisions can be based so patients have the best treatment available. After his death, the Cochrane Collaboration, a movement to encourage systematic reviews for that purpose, was named in his honor. The published literature on lumbar RF procedures includes numerous reports of case series, clinical trials, and systematic reviews showing various outcomes including total pain relief, partial pain relief, only short-term pain relief, and no relief after what are all described as “lumbar radiofrequency” treatments. None of the individual studies other than those described earlier156,157,187 are of procedures performed in the manner recognized as the standard for RF lumbar MBN, so strictly speaking, they are irrelevant to it. These irrelevant publications include reports of procedures targeting the lumbar dorsal root ganglia rather than the medial branches, procedures using pulsed radiofrequency rather than thermal radiofrequency fields, and procedures done for various indications

Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment  385

including partial relief of low back pain after single, uncontrolled intraarticular injections. Some clinicians fail to understand the difference between these studies and those of valid RF lumbar MBN, perhaps simply because the words “lumbar” and “radiofrequency” appear in their titles. The confusion is made worse by the publication of what purport to be systematic reviews, which include dissimilar studies as if they are comparable. The authors of such reviews are supposed to understand methodology and to be discriminating in selecting study reports for comparison, yet there are three so-called “systematic reviews”190,192,193 of RF procedures for spinal pain that lump together the data of widely disparate interventions and draw unwarranted conclusions. These conclusions are essentially irrelevant to RF lumbar MBN but the confusion they engender results in some patients with chronic ZJ pain being denied the treatment they need for relief, contrary to what Archie Cochrane strove to achieve. If anyone contended that apples and oranges are the same and then discussed fruit publicly as if the equality of apples and oranges is self-evident, their contention would be bound to cause controversy and the origin of the controversy would be obvious. When discussing spine interventions, including MBBs and RFMBN, only apples should be compared with apples. There are published standards for these procedures, standards set on the basis of sound, scientific evidence and agreed by clinicians experienced in their effective use. When the procedures are being evaluated for their validity and effectiveness, controversy can be avoided by considering only procedures performed in accordance with those standards, which are described fully in the ISIS practice guidelines. REFERENCES  1. Federative Committee on Anatomical Terminology. Terminologica Anatomica. New York: Thieme Medical Publishers; 1998.  2. Goldthwaite JE. The lumbo-sacral articulation: An explanation of many cases of “lumbago,” “sciatica,” and paraplegia. Boston Med J. 1911;164:365-372.  3. Ghormley RK. Low back pain with special reference to the articular facets, with presentation of an operative procedure. J Am Med Assoc. 1933;101:1773-1777.  4. Mooney V, Robertson J. The facet syndrome. Clin Orthop Relat Res. 1976;115:149-156.  5. Bogduk N. The clinical anatomy of the cervical dorsal rami. Spine. 1982;7:319-330.  6. Bogduk N, Marsland A. The cervical zygapophysial joints as a source of neck pain. Spine. 1988;13:610-617.  7. Hollinshead WH. Anatomy for Surgeons. 3rd ed. Philadelphia: Harper & Row; 1982:77-105.  8. Nordin CC, Levangie PK. Joint Structure and Function. A Comprehensive Analysis. 2nd ed. Philadelphia: F.A. Davis; 1992:128-129.  9. Delmas A, Ndjaga-Mba M, Vannareth T. Le cartilage articulaire de L4-5 et L5-S1. Comptes Rendus de l’Association des Anatomistes. 1970;147:230-234.   10. Bland JH, Boushey DR. Anatomy and physiology of the cervical spine. Semin Arthritis Rheum. 1990;20:1-20.   11. Lewin T, Moffet B, Viidik A. The morphology of the lumbar synovial intervertebral joints. Acta Morphol Neerlando-Scandinav. 1962;4:299-319.   12. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain ­patterns: I: A study in normal volunteers. Spine. 1990;15:453-457.   13. Engel R, Bogduk N. The menisci of the lumbar zygapophysial joints. J Anat. 1982;135:795-809.   14. Wyke B. Articular neurology—a review. Physiotherapy. 1972;58:94-99.   15. Bogduk N, Wilson AS, Tynan W. The human lumbar dorsal rami. J Anat. 1982;134:383-397.   16. International Spine Intervention Society. Lumbar medial branch blocks. In: Bogduk N, ed. Practice Guidelines for Spinal Diagnostic and Treatment Procedures. San Francisco: International Spine Intervention Society; 2004:47-65.

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122. Van der Donk J, Schouten JS, Passchier J, et al. The associations of neck pain with radiological abnormalities of the cervical spine and ­personality traits in a general population. J Rheumatol. 1991;18:1884-1889. 123. Symmons DPM, van Hemert AM, Vandenbroucke JP, Valkenburg HA. A longitudinal study of back pain and radiological changes in the lumbar spines of middle aged women: II. radiographic findings. Ann Rheum Dis. 1991;50:162-166. 124. Schwarzer AC, Wang SC, O’Driscoll D, et al. The ability of computed tomography to identify a painful zygapophysial joint in patients with chronic low back pain. Spine. 1995;20:907-912. 125. Ronnen HR, de Korte PJ, Brink PRG, et al. Acute whiplash injury: Is there a role for MR imaging? A prospective study of 100 patients. Radiology. 1996;201:93-96. 126. Fukuda K, Kawakami G. Proper use of MR imaging for evaluation of low back pain (radiologist’s view). Semin Musculoskelet Radiol. 2001;5:133-136. 127. Merskey H, Bogduk N, eds. Classification of Chronic Pain. Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms. 2nd ed. Seattle: International Association for the Study of Pain Press 1994:xi-xii. 128. Bonica JJ. The Management of Pain. Philadelphia: Lea and Febiger; 1953. 129. Sternbach RA. Pain Patients: Traits and Treatments. New York: ­Academic Press; 1974. 130. King W. Acute, Subacute and Chronic Pain. In: Schmidt RF, Willis Jr WD, eds. Encylopedic Reference of Pain. Berlin: Springer-Verlag; 2007:35-36. 131. Borghouts JAJ, Koes BW, Bouter LM. The clinical course and prognostic factors of non-specific neck pain: A systematic review. Pain. 1998;77:1-13. 132. Indahl A, Velund L, Reikerås O. Good prognosis for low back pain when left untampered. Spine. 1995;20:473-477. 133. McGuirk B, King W, Govind J, et al. Safety, efficacy, and cost-­ effectiveness of evidence-based guidelines for the management of acute low back pain in primary care. Spine. 2001;26:2615-2622. 134. Bogduk N, Derby R, Aprill C, et al. Precision diagnosis of spinal pain. In 8th World Congress on Pain, Refresher Course Syllabus Seattle: International Association for the Study of Pain Press; 1996:313-323. 135. Hove B, Gyldensted C. Cervical analgesic facet joint arthrography. Neuroradiology. 1990;32:456-459. 136. Wilson PR. Thoracic facet syndrome: A clinical entity? Pain. 1987; 4(suppl):S87. 137. Barnsley L, Bogduk N. Medial branch blocks are specific for the ­diagnosis of cervical zygapophysial joint pain. Reg Anesth. 1993;18:343-350. 138. Dreyfuss P, Schwarzer AC, Lau P, Bogduk N. Specificity of lumbar medial branch and L5 dorsal ramus blocks. A computed tomographic study. Spine. 1997;22:895-902. 139. Lord SM, McDonald GJ, Bogduk N. Percutaneous radiofrequency neurotomy of the cervical medial branches: A validated treatment for cervical zygapophysial joint pain. Neurosurg Q. 1998;8:288-308. 140. Bogduk N. International Spinal Injection Society guidelines for the performance of spinal injection procedures. Part 1: Zygapophysial joint blocks. Clin J Pain. 1997;13:285-302. 141. International Spine Intervention Society. Cervical medial branch blocks. In: Bogduk N, ed. Practice Guidelines: Spinal Diagnostic and Treatment Procedures. San Francisco: International Spine Intervention Society; 2004:112-137. 142. Barnsley L, Lord SM, Wallis BJ, Bogduk N. False-positive rates of cervical zygapophysial joint blocks. Clin J Pain. 1993;9:124-130. 143. Barnsley L, Lord S, Bogduk N. Comparative local anaesthetic blocks in the diagnosis of cervical zygapophysial joint pain. Pain. 1993; 55:99-106. 144. Lord SM, Barnsley L, Wallis BJ, et al. Percutaneous radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl J Med. 1996;335:1721-1726.

36

388  Spine 145. Govind J, King W, Bailey B, Bogduk N. Radiofrequency neurotomy for the treatment of third occipital headache. J Neurol Neurosurg ­Psychiatry. 2003;74:88-93. 146. Lord SM, Barnsley L, Bogduk N. The utility of comparative local anesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical zygapophysial joint pain. Clin J Pain. 1995;11:208-213. 147. Verrills P, Mitchell B, Vivian D, et al. The incidence of intravascular penetration in medial branch blocks: cervical, thoracic, and lumbar spines. Spine. 2008;33:E174-E177. 148. Chua WH, Bogduk N. The surgical anatomy of thoracic facet denervation. Acta Neurochir. 1995;136:140-144. 149. International Spine Intervention Society. Thoracic medial branch blocks. In: Bogduk N, ed. Practice Guidelines: Spinal Diagnostic and Treatment Procedures. San Francisco: International Spine Intervention Society; 2004:330-347. 150. International Spine Intervention Society. Lumbar medial branch blocks. In: Bogduk N, ed. Practice Guidelines: Spinal Diagnostic and Treatment Procedures. San Francisco: International Spine Intervention Society; 2004:47-65. 151. Dreyfuss P, Schwarzer AC, Lau P, Bogduk N. The target specificity of lumbar medial branch and L5 dorsal ramus blocks: A computed tomography study. Spine. 1997;22:895-902. 152. Schwarzer AC, Aprill CN, Derby R, et al. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophysial joints. Pain. 1994;58:195-200. 153. Manchikanti L, Pampati V, Fellows B, Bakhit CE. The diagnostic validity and therapeutic value of lumbar facet joint nerve blocks with or without adjuvant agents. Curr Rev Pain. 2000;4:337-344. 154. Bogduk N. On the rational use of diagnostic blocks for spinal pain. Neurosur Q. 2009;19:88-100. 155. Kaplan M, Dreyfuss P, Halbrook B, Bogduk N. The ability of lumbar medial branch blocks to anesthetize the zygapophysial joint. A physiologic challenge. Spine. 1998;23:1847-1852. 156. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophysial joint pain. Spine. 2000;25:1270-1277. 157. Nath S, Nath CA, Pettersen K. Percutaneous lumbar zygapophysial (facet) joint neurotomy using radiofrequency current, in the management of chronic low back pain. A randomized double-blind trial. Spine. 2008;33:1291-1297. 158. McCormick CC. Arthrography of the atlanto-axial (C1-C2) joints: Technique and results. J Intervent Radiol. 1987;2:9-13. 159. International Spine Intervention Society. Lateral atlanto-axial joint blocks. In: Bogduk N, ed. Practice Guidelines: Spinal Diagnostic and Treatment Procedures. San Francisco: International Spine Intervention Society; 2004:138-151. 160. Ehni G, Benner B. Occipital neuralgia and the C1-2 arthrosis syndrome. J Neurosurg. 1984;61:961-965. 161. Busch E, Wilson PR. Atlanto-occipital and atlanto-axial injections in the treatment of headache and neck pain. Reg Anesth. 1989;14(suppl 2):45. 162. Joseph B, Kumar B. Gallie’s fusion for atlantoaxial arthrosis with occipital neuralgia. Spine. 1994;19:454-455. 163. Ghanayem AJ, Leventhal M, Bohlman HH. Osteoarthrosis of the atlanto-axial joints. Long-term follow-up after treatment with arthrodesis. J Bone Joint Surg Am. 1996;78:1300-1307. 164. Dreyfuss P, Rogers J, Dreyer S, Fletcher D. Atlanto-occipital joint pain. A report of three cases and description of intraarticular joint block technique. Reg Anesth. 1994;19:344-351. 165. Lippit AB. The facet joint and its role in spine pain. Management with facet joint injections. Spine. 1984;9:746-750. 166. Lau LSW, Littlejohn GO, Miller MH. Clinical evaluation of intra-articular injections for lumbar facet joint pain. Med J Aust. 1985;143:563-565. 167. Lynch MC, Taylor JF. Facet joint injection for low back pain. A clinical study. J Bone Joint Surg Br. 1986;68:138-141. 168. Murtagh FR. Computed tomography and fluoroscopy guided anesthesia and steroid injection in facet syndrome. Spine. 1988;13:686-689.

169. Barnsley L, Lord SM, Wallis BJ, Bogduk N. Lack of effect of intraarticular corticosteroids for chronic pain in the cervical zygapophyseal joints. N Engl J Med. 1994;330:1047-1050. 170. Carette S, Marcoux S, Truchon R, et al. A controlled trial of corticosteroid injections into facet joints for chronic low back pain. N Engl J Med. 1991;325:1002-1007. 171. Peterson TH. Injection treatment for back pain. Am J Orthop. 1963; 5:320-325. 172. Schuster GD. The use of cryoanalgesia in the painful facet syndrome. J Neurol Orthop Surg. 1982;3:271-274. 173. Rees WES. Multiple bilateral percutaneous rhizolysis. Med J Aust. 1975;1:536-537. 174. Shealy CN. Percutaneous radiofrequency denervation of spinal facets. Treatment for chronic back pain and sciatica. J Neurosurg. 1975;43:448-451. 175. Bogduk N, Long D. The anatomy of the so-called “articular nerves” and their relationship to facet denervation in the treatment of lowback pain. J Neurosurg. 1979;51:172-177. 176. International Spine Intervention Society. Percutaneous radiofrequency cervical medial branch neurotomy. In: Bogduk N, ed. Practice Guidelines: Spinal Diagnostic and Treatment Procedures. San Francisco: International Spine Intervention Society; 2004:249-284. 177. Lord SM, Barnsley L, Bogduk N. Percutaneous radiofrequency neurotomy in the treatment of cervical zygapophyseal joint pain: a caution. Neurosurgery. 1995;36:732-739. 178. Bassett K, Sibley LM, Anton H, et al. Percutaneous radio-frequency neurotomy treatment of chronic cervical pain following whiplash injury: Reviewing evidence and needs. Vancouver: University of British Columbia Centre for Health Services and Policy Research; 2001, ­British Columbia Office of Health Technology Assessment monograph report 01:5T. 179. Wallis BJ, Lord SM, Bogduk N. Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy: a randomised, double-blind, placebo-controlled trial. Pain. 1997;73:15-22. 180. McDonald GJ, Lord SM, Bogduk N. Long-term follow-up of patients treated with radiofrequency neurotomy for chronic neck pain. Neurosurgery. 1999;45:61-68. 181. Barnsley L. Percutaneous radiofrequency neurotomy for chronic neck pain: outcomes in a series of consecutive patients. Pain Med. 2005;6:282-286. 182. International Spine Intervention Society. Percutaneous radiofrequency lumbar medial branch neurotomy. In: Bogduk N, ed. Practice Guidelines: Spinal Diagnostic and Treatment Procedures. San Francisco: International Spine Intervention Society; 2004:188-218. 183. Lau P, Mercer S, Govind J, Bogduk N. The surgical anatomy of lumbar medial branch neurotomy (facet denervation). Pain Med. 2004;5:289-298. 184. van Kleef M, Barendse GA, Kessels A, et al. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine. 1999;24:1937-1942. 185. Tekin I, Mirzai H, Ok G, et al. A comparison of conventional and pulsed radiofrequency denervation in the treatment of chronic facet joint pain. Clin J Pain. 2007;23:524-529. 186. Burnham RS, Holitski S, Dinu I. A prospective outcome study on the effects of facet joint radiofrequency denervation on pain, analgesic intake, disability, satisfaction, cost, and employment. Arch Phys Med Rehabil. 2009;90:201-205. 187. Gofeld M, Jitendra J, Faclier G. Radiofrequency denervation of the lumbar zygapophysial joints: 10-year prospective clinical audit. Pain Physician. 2007;10:291-300. 188. Manchikanti L, Singh V, Vilims BD, et al. Medial branch neurotomy in management of chronic spinal pain: systematic review of the evidence. Pain Physician. 2002;5:405-418. 189. Datta S, Lee M, Falco FJ, et al. Systematic assessment of diagnostic accuracy and therapeutic utility of lumbar facet joint interventions. Pain Physician. 2009;12:437-460.

Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment  389 190. Niemistö L, Kalso E, Malmivaara A, et al. Radiofrequency denervation for neck and back pain: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine. 2003;16:1877-1888. 191. Cochrane AL. Effectiveness and Efficiency. Cambridge, UK: Cambridge University Press; 1972.

192. Geurts JW, van Wijk RM, Stolker RJ, Groen GJ. Efficacy of radiofrequency procedures for the treatment of spinal pain: a systematic review of randomized clinical trials. Reg Anesth Pain Med. 2001;26:394-400. 193. Slipman CW, Bhat AL, Gilchrist RV, et al. A critical review of the evidence for the use of zygapophysial injections and radiofrequency denervation in the treatment of low back pain. Spine J. 2003;3:310-316.

36

Sacroiliac Joint Pain: ­Procedures for Diagnosis and Treatment

37

Bruce Mitchell, MM, BS, FACSP, and David G. Vivian, MM, BS, FAFMM

Over the last 2 decades, the sacroiliac joint (SIJ) has increasingly been recognized as an anatomic source of pain that figures in the differential diagnosis of a patient presenting with low back pain (LBP) and/or buttock pain with or without more distant referred pain.1-7 Because the SIJ is innervated, it can be a source of pain.2,8-13 Because SIJ pain refers into the buttock and iliac crest near the posterior-superior iliac spine, and also into the groin, abdomen, and leg including the foot,14,15 it can be confused with referred pain from other sources, particularly from the lumbar intervertebral disc, lumbar zygapophysial joint (ZJ), and the hip joint. Additionally, because of its propensity for referral into the leg, SIJ pain can be confused with radicular pain. Thus, it is essential that the clinician recognizes these potentially confounding features and takes adequate steps to differentiate between SIJ pain and other pain presentations. In the early 1900s, the SIJ was thought to be the principal source of LBP,16 and an important cause of “sciatica.”17 Subsequently, and particularly after the discovery of the disc prolapse, it was considered that the lumbar spine—and in particular the lumbar intervertebral disc—was responsible for most back problems.17 Acknowledgment of the SIJ as a source of pain in the ensuing decades commenced in rheumatologic literature, but this largely related to seronegative arthropathies and case reports of various rare infections and tumors.18,19 Subsequently there have been substantial developments in the basic sciences relating to the SIJ, initially and primarily in the osteopathic, physiotherapy, and chiropractic literature,18,19 and later in biomechanical and radiologic­ literature.20-26 The SIJ was overlooked as a possible pain generator outside of the inflammatory population perhaps because it was deep and inaccessible to specific accurate injection prior to the development of C-arm fluoroscopy, and because clinical examination tests had poor sensitivity and specificity. The advent of imagingcontrolled diagnostic interventions has allowed for a more rational approach to diagnosis, and as a result, there is again an increasing awareness that the SIJ is an important cause of LBP and referred pain into the pelvis and leg. It is now estimated that the SIJ may be the cause of between 15% and 38% of all cases of LBP.4,27-30 The increased awareness of the potential for the SIJ to be a source of pain has not as yet translated into proven treatments. The literature concerning SIJ interventional treatment is sparse.1,31-35 The SIJ can be a source of pain in various disease states. This chapter is restricted to so-called mechanical disorders, and does not discuss other conditions such as inflammatory conditions (e.g.,

ankylosing spondylitis), infection, and fracture. However, the clinician needs to exclude these important red-flag causes of SIJ pain when making a diagnosis.

Anatomy and Biomechanics The SIJ is the articulation between the triangular sacrum and the two ilia. It is a true diarthrodial synovial joint, and is unlike any other joint in the body. Only the ventral third of the joint is a true synovial joint with a joint capsule and synovial cells;36 the remainder is composed of three ligaments,37 the ventral sacroiliac ligament, the interosseous sacroiliac ligament, and the posterior sacroiliac ligament.38 From fetal life onward, the iliac surface is fibrocartilage and the sacral surface is hyaline cartilage. Subsequent arthrosis of the joint tends to affect the fibrocartilaginous iliac side more than the sacral hyaline cartilage.39 The dorsal transition between the ligamentous and synovial components shows marked individual variability including osseous clefts, cartilage and subchondral defects, and vascular connective tissue in the bone marrow.36 Furthermore, aging is accompanied by extensive ridging in the interosseous region of the sacrum and ilium to the extent that it is present in 100% of those 55 years or older and also by ossification of the central interosseous region of the SI ligament in 60%, making it likely that by the sixth decade of life there is little or no movement in the SIJ.40 Other degenerative changes such as marginal osteophytes are not uncommon by the start of the fifth decade, at least unilaterally.41 The articular cartilage of the SIJ does not appear to degenerate in a similar manner to other synovial joints in which articular cartilage defects result in bony ankylosis. The SIJ articular cartilage is maintained even in the elderly; it seems that fibrous tissues contribute most to ankylosis so that with aging there is interposition of fibrocartilage-like tissues within the joint (complete fibrous ankylosis).42 Bony fusion seems to occur only in ankylosing spondylitis.43 Degenerative changes and intraarticular SIJ ankylosis are substantially more common in men than women.43-45 The sacrum contains four foraminal pairs on either side, S1 to S4. Each pair has a ventral and dorsal aperture. On x-ray, the ventral component of the foramen is the most obvious; the smaller dorsal foramen can be difficult to visualize. It is important to recognize this when performing imaging-guided procedures into a sacral foramen. The dorsal component of each foramen may be difficult to visualize on a static image particularly because of the 391

392  Spine

Figure 37-1  Sacral dorsal and ventral foraminal views. The dorsal foramen can be difficult to see on radiographs. The obvious foramen here is the ventral foramen. The needle in both images is in the dorsal foramen. The image on the right, has been “obliqued” to the right to separate the foramen.

superimposition of the larger ventral component and from bowel gas. However, with the use of CT scan or more preferably a C-arm image intensifier, the dorsal component can be identified. With the C-arm, this is achieved by varying the amount of obliquity and observing that the more superficial dorsal component moves to a greater extent relative to the deeper ventral component (Fig. 37-1). The synovial part of the joint is more prominent caudally. At the level of the S1 foramen, the ventral 25% of the joint is synovial; at S2, the ventral 50% to 75% is synovial and at S3, 100% of the SIJ is synovial.46 The pelvis is made up of three bones, with the sacrum positioned as the keystone in an arch from femur to femur (Fig,37-2). The stability of the sacrum within the pelvis is dependant on (1) the shape and orientation of the sacrum and its articulations with the ilia, (2) the integrity of the ligamentous structure around the joint, and (3) the extent of muscular compression across the joint. Variations in the shape and orientation of the sacrum and its articulations are rarely a problem except when these aberrations are quite extreme; for example, after pelvic fractures and in some congenital conditions. The ligamentous function of the SIJ is dependant on intact, stable ligaments and the orientation of the sacrum. The sacrum pivots in a sagittal plane around its true articular joint surface by between 6 and 11 degrees. Tilting of the superior sacrum in an anterior direction is called sacral nutation. This is its normal position, encouraged by the lumbar lordosis. Excess nutation can occur. Superiorly, such excess nutation is limited directly by the deep interosseous and long dorsal ligaments and indirectly by the iliolumbar ligament. Inferiorly, it is limited by the sacrococcygeal and sacrotuberous ligaments. If all of these ligaments are intact, nutation of the sacrum has the benefit of helping to pull the pelvic ring closed, thereby compressing the SIJs. This, the so-called “locked” position of the pelvis, has great biomechanical strength with force transfer occurring primarily through a well supported and mechanically advantaged joint surface and it ligaments. This passive locking mechanism, depending on the shape of the keystone and the integrity of the articular capsule and surrounding ligaments, is called form ­closure of the SIJ. Conversely, tilting of the superior sacrum in a posterior direction is called counter nutation. It has the effect of “unlocking” the pelvis and creating a loss of passive compression across the SIJs. The ligaments and capsule of the SIJ cannot, however, provide adequate compression across the joint surface on their own. The primary compressors of the SIJs are muscular; their actions are termed force closure of the SIJ. Three main muscle groups have been

Figure 37-2  Sacral keystone. The arch has long been recognized as the perfect structure for force transfer from two pillars to one. Shown here is the pelvic arch with the sacrum as the keystone.

identified: (1) muscles of the pelvic floor, (2) transverse abdominis, and (3) a posterior sling consisting of latissimus dorsi through the thoracolumbar fascia to the contralateral gluteals.20-22,47-56

Innervation Sacroiliac joint innervation is important because the only method for making a diagnosis of SIJ origin pain is anesthetic block of the joint or its nerve supply, and one possible 53-56method of treatment is radiofrequency (RF) treatment directed at target nerves. The SIJ is definitely innervated and it can be a source of pain. The periarticular tissues of the SIJ contain mechanoreceptors and nociceptors.2 Nerve fibers varying from 0.2 micron to 2.5 microns in diameter end in five morphologically different terminals and these terminals are present in the SIJ capsule and adjacent ligaments.9 Substance P and calcitonin gene-related peptide (CGRP) immunoreactive nerve fibers have been found in the anterior SIJ capsule and interosseous ligament,13 the superficial layer of sacral and iliac cartilage, and the surrounding ligamentous structures.12 Nerves supplying the SIJ are distributed not only to the superficial and deep dorsal sacroiliac ligaments, but also to the sacrotuberous and sacrospinous ligaments;

Sacroiliac Joint Pain: Procedures for Diagnosis and Treatment  393

S1

S2

S3

Figure 37-3  Sacral innervation. The dorsal foramina are outlined with the courses of the lateral branches arising from the foramen outlined. A needle has been placed in the inferior edge of the right S1 dorsal foramen. (Based on the dissections of Dr. Frank Willard. Reproduced with his permission.)

the dorsal rami continue their course laterally, sandwiched between superficial and deep portions of sacroiliac ligaments, and pierce the origin of the gluteus maximus muscle.57 It is considered that the synovial component of the SIJ has a different innervation to the posterior ligamentous component. The synovial joint is likely to be innervated mainly by ventral sources;8,9 its upper ventral portion is mainly innervated by the L5 ventral ramus and the lower ventral portion by the S2 ventral ramus or by branches from the sacral plexus.9 The synovial component has minimal innervation by the sacral dorsal rami.58 The dorsal sacroiliac ligaments are innervated by at least the L5 dorsal ramus and lateral branches of the S1-S3 dorsal rami. The L4 medial branch may be involved. The upper dorsal ligamentous structures are innervated by the L5 dorsal ramus; the lower dorsal ligaments by nerves arising from a plexus composed of lateral branches of the dorsal rami of the sacral nerves.9 These nerves range from 0.292 mm to 0.997 mm in diameter, and the nerves supplying both the synovial and ligamentous components of the SIJ complex have similar diameters.9 The lateral branches of the sacral dorsal rami emerge from the sacral foramina in a varied array, radiating cephalad, transverse, or caudad.58 When they emerge, they do not run in a constant plane,11,58,59 but run across the dorsal sacrum either through, superficial to, or deep to the dorsal sacroiliac ligament at a variable depth of up to 1 cm superficial to bone (Fig. 37-3).58,60

Pathophysiology As noted previously, the SIJ is innervated and has the potential to be a source of pain. It can become painful as a result of both intrinsic and extrinsic factors. Intrinsic mechanisms include definitive biomedical processes such as sacroiliitis and tumors. These constitute

red-flag conditions and are not covered in this chapter. The other intrinsic mechanism considered to be a risk factor in SIJ origin pain relates to aberration of biomechanical function. The technical terms used to describe these biomechanical features are form closure and force closure. Poor form closure of the SIJ is caused by inefficient bony structure/alignment, absent or stretched SIJ ligaments, or sacral counter nutation. Poor force closure is considered to arise through pain inhibition and poor firing of the compressive muscles (Fig. 37-4).61-67 It is likely that long-term lack of force closure across the SIJ can lead to increased strain on the ligamentous structures, which, over time may lengthen and cause further loss of pressure across the joint. Such a joint may then be resistant to muscular retraining. Extrinsic mechanisms causing loss of form or force closure include trauma (macro or repetitive microtrauma), infection, and pregnancy.20,47,63,68-73 Pain in the region of the SIJ is not uncommon after posterior iliac graft harvesting.74 It occurs in 6% to 39% in patients who have had iliac grafting for spinal fusion.75,76 One possible cause is sacroiliac joint instability, caused by ligamentous disruption or violation of the synovial part of the SIJ during surgery. In patients who have had posterior iliac grafting and have persistent SIJ region pain with CT scan evidence of synovial disruption, SIJ degeneration is more prevalent on CT.77 SIJ pain is also not uncommon after spinal fusion. The prevalence of SIJ pain, diagnosed on the basis of 75% or more pain relief with local anesthetic block, in one group of patients with significant and chronic LBP postlumbar fusion surgery was found to be 35%,78 a figure that seems to be similar to that in other reports.79 Bone scan does not assist in the diagnosis of postfusion SIJ origin pain using local anesthetic as the diagnostic tool; however, clinical features that are somewhat predictive include pain that is different to the prefusion pain, particularly if it commences some time after the fusion has been performed.78 SIJ pain postfusion occurs as fusion increases the computed sacral angular motions and the average stress on the SIJ articular surface motion particularly in combined L4-5 and L5-S1 fusion.79 This can lead not only to an increased chance of pain, but also to premature SIJ degeneration; the prevalence of CT scan determined SIJ degeneration over a 5-year period postlumbar fusion was found to be 75% in one study that found a prevalence of only 38% in a matched control group.80 Consistent with the finding that L5-S1 fusion had the more significant biomechanical effect, the prevalence of SIJ degeneration was higher if the L5-S1 segment was included in the fusion.80 Sacroiliitis is characterized by chronic inflammation within the joint and the deep interosseous ligament, which forms the posterior capsule and is the largest syndesmosis in the body. Both hyperparathyroidism and repetitive shear stress injuries in athletes can mimic the presentation of sacroiliitis.81 In a study of long-term outcomes from SIJ radiofrequency neurotomy (RFN), SIJ pain was considered to be idiopathic in 30% of cases, and to derive from motor vehicle accidents in 9%, from a fall or slip in 24%, from overload or a work injury in 26%, and from other incidents in 11% of cases.82

Clinical Presentation and Diagnosis The diagnosis of SIJ pain is predicated on diagnostic anesthetic injection because there are no other clinical or radiologic correlations that have been found to be reasonable surrogates. The most

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Form closure

Force closure

significant feature on clinical assessment of a patient considered to have SIJ origin pain is the site of pain; if the patient points to the posterior superior iliac spine (PSIS), then the pain is more likely to derive from the SIJ.28 Clinical examination has possible utility when examination findings are considered collectively. Radiologic findings are of no particular use other than in the exclusion of some red-flag conditions. The International Association for the Study of Pain (IASP) has proposed a three-part criteria for the diagnosis of SIJ pain.83 In particular, diagnosis requires the following: 1. The patient has pain in the region of the SIJ 2. The patient’s pain is reproduced by clinical tests that selectively stress the joint 3. The patient’s pain is completely relieved by selective delivery of local anesthetic Site of Pain In asymptomatic subjects, noxious stimulation of the SIJ evokes pain in the low back, buttock, and upper posterior thigh.4 In patients with SIJ pain established by fluoroscopically guided SIJ injection, 94% described buttock pain, 72% described lower lumbar pain, 14% described groin pain, 50% described associated lower-extremity pain, 28% described leg pain distal to the knee, and 14% reported foot pain.14 However, as noted, the most prominent site of pain presentation for SIJ pain is pain over the PSIS.28 SIJ pain rarely extends above L5.28 SIJ origin pain has a similar referral pattern to pain derived from the lumbar spine and from the hip joint,14,28 and thus, analysis of pain patterns is not in itself a reliable diagnostic factor.84 Type of Pain SIJ pain can present with local PSIS pain and/or somatic referred pain. Local SIJ region pain can be deep and aching, but it can also be sharp and activated by movement. Somatic referred pain is generally described as diffuse, aching, and poorly localized. It is different from typical lumbar radicular pain, which is generally described as long, thin, sharp lancinating pain that can concentrate distally.85 Because SIJ-referred pain can extend into the leg, it can be confused with radicular pain, potentially leading to unnecessary spinal treatment.17,86 If the predominant pain is radicular, it is most likely to arise from the lumbar spine owing to disc prolapse or canal stenosis. However, it is not impossible for lumbosacral radicular pain

Functioning sacroiliac joint

Figure 37-4  Form and force closure. Force transfer cannot occur across the sacroiliac joint without proper form closure and force closure. Absence of either can lead to shearing forces across the joint.

to be caused by SIJ pathology. In one series, ventral capsule disruption was present in 70% of patients diagnosed with SIJ pain by intraarticular block.30 Joint injury, if associated with inflammation, can theoretically be associated with extrasacral perineural inflammation and pain. It is also important to distinguish neuropathic pain from somatic referred pain. Neuropathic pain typically presents with descriptors such as burning, buzzing, and tingling, and has clinical features including allodynia. It can occur in association with somatic referred pain.85,86 Although uncommon, lumbosacral plexopathy, which is defined as neurologic deficit derived from the lumbosacral plexus, is more common in patients after sacral fractures than it is among the entire population of patients with pelvic and acetabular fractures.87 It stands to reason that SIJ trauma and pain can be associated with local neural damage, and hence, neuropathic pain. Fortin described five patterns of contrast medium extravasation after fluoroscopically guided SIJ injections by viewing postarthrography CT in 76 patients with LBP, of whom 61% displayed extravasation.3 It seems that extravasation does occur dorsally into the dorsal S1 foramen, superiorly at the sacral alar level to the L5 epiradicular sheath, and ventrally to the lumbosacral plexus, making it possible for local neural structures to be insulted by SIJ inflammation.

Clinical Examination The validity of physical examination tests is reduced because they tend to stress adjacent soft tissue structures as well as the lumbar spine and hips.68 Singular examination tests such as palpation and movement tests are generally considered to be unhelpful in the diagnosis of SIJ pain.27,37,68,88,89 However, combined tests may be useful. Synovial SIJ pain can be predicted when three of five pain provocation tests are positive with a sensitivity and specificity of 91% and 78%, respectively, and a consequent likelihood ratio of 4.1.90-95 Specificity improves with the absence of centralization of pain. The tests used are: 1. The distraction test 2. Posterior pelvic pressure provocation (P4) 3. Gaenslen’s test 4. Compression test 5. Sacral thrust test

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It is unknown if these tests can predict ligamentous sources of SIJ pain; clinical examination has not been assessed using ligament injection as the criterion standard. These tests individually can be positive in up to 20% of the asymptomatic population.96 The SI joint is more likely to be the source of pain if the following occur: 1. In identifying the site of pain, the patient points to the posterior superior iliac spine (buttock dimple) 2. Pain is predominantly below the L5 level28 3. Sacral sulcus is tender Tests for SIJ instability have been proved reliable particularly in the postpartum population, but there is no data supporting their efficacy in the management of SIJ pain, except in the postpartum population.51,52,73,97-99 Multiple authors raise the concept of SIJ dysfunction, where the self-locking mechanism of the SIJ complex fails due to a loss of form and/or force closure.20-22,47-56,61-64,66,69-73,97-101 The tests used to assess SIJ dysfunction are reliable and valid.49-52 The presence of SIJ dysfunction is proposed by these authors as a putative cause of SIJ pain. However, although outcome studies on treating this SIJ dysfunction show significant improvements in disability, changes in pain are less impressive.61,64,100,102

Imaging The diagnosis of SIJ origin pain is difficult because there are no valid or reliable correlations between imaging changes and SIJ pain. Imaging cannot be used as a criterion standard for diagnosis or as a basis on which to assess the validity of treatment. In one study, diagnostic CT-guided intrasynovial SIJ injections had a sensitivity of 57.5 %, a specificity of 69%, and a consequent poor likelihood ratio of 1.9,75 thus negating the use of CT in a presentation of putative SIJ origin pain except to rule out red-flag conditions. Bone scan has a very low sensitivity but a high specificity for SIJ pain diagnosed with diagnostic blocks, and is not worth performing.103 Similarly, plain radiography and MRI cannot reliably detect non– red-flag SIJ origin pain.28 Changes are often noted on imaging but they are not clinically significant. For example, the CT appearance of the SIJ is closely related to patient’s age, gender, BMI, and in women, parity.104 The widths of the SIJ space and of the subchondral sclerosis on the iliac and sacral sides narrow over time; they were measured to be 2.3±0.4mm, 2.5±1.6mm and 1.4±0.5 mm, respectively, in patients younger than 40 years of age and 1.9±0.2 mm, 3.6±2.1 mm and 2.3±1.1 mm, respectively, in patients older than 40 years of age.104 SIJ changes include increased joint space narrowing and loss of joint space uniformity. Subchondral sclerosis appears to be wider and less uniform in the elderly.104 Osteophytes are present even in younger patients and their prevalence increases with advancing age.104 CT has identified six anatomic variants termed accessory joints (19.1% of assessed SIJs), iliosacral complex (5.8%), bipartite iliac bony plate (4.1%), crescent-like iliac bony plate (3.7%), semicircular defects at the sacral or iliac side (3%), and ossification centers (0.6%).105

Diagnostic Injections Properly conducted SIJ injection is considered the criterion standard diagnostic technique.27 Intricacies and subtleties in this diagnostic approach to SIJ pain need to be understood. Diagnostic

injections can be performed using various forms of imaging guidance such as C-arm fluoroscopy, ultrasound, and CT. More recently, image fusion, in which a software technology matching real-time ultra­sonography and a previously obtained CT, has been tested and found to be accurate, but it is slow, taking on average about 20 minutes.106 MR-guided sacroiliac and other spinal injections can also be performed in open high-field MRI using fast TSE sequence designs.107 However, although there was a reported accuracy of drug delivery of 100% for nerve root injections, the accuracy for ZJ and SIJ delivery was only 87%, and the average time taken was 29 minutes (range 19 to 67 minutes).107 Site of Injection There are two components to the SIJ and it appears that SIJ pain can be established as the likely source of pain only if both components are assessed. The need to assess both components, however, should be predicated on the treatment that might ensue from such a diagnostic approach. As discussed earlier, the ligamentous component of the joint is innervated by at least the dorsal ramus of L5, and certainly by the lateral branches of the dorsal rami that emerge from the S1, S2, and S3 foramina. If the treatment is to be RFN of these nerves, then it stands to reason that the diagnostic injection should be directed at these nerves. As the synovial SIJ is innervated ventrally, nerve blocks cannot be used as a diagnostic test for synovial SIJ pain; lateral branch blocks do not anesthetize the synovial SIJ.58 The only method that can be used to diagnose synovial SIJ pain is intraarticular injection. This might be used as a test if steroid or other material is to be injected into the synovial component, or if a surgical procedure such as SIJ is considered relevant. Because the sacral lateral branches run at a variable depth and have a variable course over the sacrum, multisite, multidepth, sacral lateral branch blocks are recommended; this method renders the interosseous and dorsal sacral ligaments insensate in 70% of subjects.58,60 Another option to lateral branch blocks is to inject into the ligamentous component of the SIJ itself using contrast to exclude extraneous injection. Number of Injections Are controlled blocks required? In high prevalence conditions, such as in the search for ZJ pain in a population of post-whiplash neck pain patients, it has been established that double blocks are required; one with a short-acting anesthetic and another with a longer acting anesthetic.108,109 As the prevalence of an index cohort decreases within a tested population, the chances of false-positive findings with single blocks rises substantially. In such circumstances, triple blocks may be necessary, with the addition of a placebo arm. The use of a control block is recommended by Hansen and colleagues because their review of two studies with 54110 and 120111 patients found a false-positive rate for the technique of between 20% and 22% for a single block.34 Conversely, Mitchell and coworkers assessed 1146 consecutive double-block technique combined intraarticular and ligamentous injections over a 2.5-year period and found that the first block predicted the control block result in 85% of cases for a positive block and in 87% for a negative block.112 Use of Contrast Contrast is required in all instances because it confirms that the injectate is in the joint or ligament or adjacent to the nerve, and it excludes intravascular injection or extravasation into surrounding tissues. Ventral extravasation has been reported in as many as 61%

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of all SIJ injections;3 if so, false-positive blocks occur because of the proximity of sheaths of the adjacent nerve trunks or roots, including the lumbosacral trunk and the L5 and S1 nerve roots.89 Thus, when local anesthetic is injected into the SIJ, a possible short-term complication is leg weakness for the duration of the local anesthetic action. Any injection into the SIJ without contrast, even under CT, should be viewed with skepticism, at least in respect to its diagnostic utility. Volume In intraarticular SIJ injection, the accepted maximum volume is 2.5  mL,58 but less should be injected if there is increased pain or pressure. Ligamentous injection volume is about 2 mL. The multisite, multidepth injections onto the lateral branches of the dorsal rami from S1 to S3 require 0.2 mL per infiltration.58 Interpretation In research, it is generally considered that the criterion for a positive block should be 100% pain relief or very close to it. In clinical practice, reduction of VAS in the order of 80% may be considered a positive finding.16

Summary Pain from either or both components of the SIJ can be suspected when the presenting pain concentrates over the SIJ. A combination of physical tests may predict a positive diagnostic block regimen. Imaging tests are not helpful in diagnosing such pain, but they may be helpful in excluding red-flag conditions. Controlled blocks are used as the criterion standard for diagnosis.

Treatment A number of modalities are available for the treatment of putative SIJ pain. At present, however, the literature regarding the efficacy of each is limited. By the time a target-specific diagnosis is made by injection, it is likely that the pain will have failed numerous trials of conservative management including physical therapy, medications, bracing, kinesiology, and exercise; it is assumed this includes targeting specific retraining of the pelvic floor, transverse abdominis, and the posterior sling. The diagnostic injection into the joint or the dorsal interosseous ligament typically includes cortisone and may be therapeutic in itself. If it is not, percutaneous RFN can be considered. Stabilization of the joint through prolotherapy or fusion may also be appropriate.

Efficacy Corticosteroid Injection Sacroiliac corticosteroid injections have not been tested with randomized controlled trials (RCTs). Accordingly, a systematic review concluded that the evidence supporting therapeutic injection is limited.34 However, many case series studies report that intrasynovial SIJ corticosteroid injections provide good to excellent pain relief with a duration of up to 10 months.37 A retrospective practice audit of 155 patients who underwent diagnostic and therapeutic fluoroscopically guided contrast confirmed SIJ injections with local anesthetic and corticosteroid were considered positive if they produced 50% or greater pain relief during the local anesthetic block phase and if there was subsequent pain relief for 2 weeks or more. Of the 155 patients, 69 (45%) had

previous lumbar surgery and 120 (77%) were positive responders over a mean duration follow-up period of 44 months (range 26 to 101 months).113 The positive responders received a mean of 2.7 injections per patient. Forty patients required one injection only, 29 required two, 22 required three, and 27 required four or more. The mean duration of response for those receiving more than one injection was 9.3 months per injection (range 1 to 58 months). There were no adverse events. In practice, corticosteroid and other injections can be inserted into either or both the synovial or ligamentous component of the SIJ. Intrasynovial etanercept is now injected in the treatment of ankylosing spondylitis: a case series reported that it improved both clinical features and morphologic parameters significantly, and that it was safe and cost effective.114 Radiofrequency Neurotomy Sacroiliac treatment using cooled RFN has been assessed positively with an RCT.115,116 In this trial, 28 patients were equally divided into treatment with cooled RFN and sham treatment groups. Patients in the treatment group received denervation of the L4 medial branch, the L5 dorsal ramus, and at the S1-3 lateral branches. The proportion of participants experiencing greater than 50% pain relief at 1, 3, and 6 months postoperatively in the treatment cohort was 79%, 64%, and 57%, respectively; in the placebo group, the proportion of participants experiencing greater than 50% pain relief at 1 and 3 months postoperatively was 14% and 0%, respectively. Subsequently, 11 patients crossed over to RFN treatment, and of these, at 1, 3, and 6 months the proportion of patients reporting improvement was 64%, 55%, and 36%, respectively. The treatment effect was seen to diminish by 12 months; at that time only 14% (two patients) of the treatment group had persistent pain relief. It was suggested that larger studies were needed to further assess the efficacy of SIJ RFN. The same group reported on 77 patients who underwent lateral branch SIJ RFN treatment using a 50% reduction in pain at 6 months as a successful outcome. Of these, 40 (52%) obtained a positive outcome. The multivariate analysis found that predictors of an unsuccessful outcome were older than 65 years and experienced pain radiating below the knee. They also noted that cooled, rather than conventional RFN, was associated with a higher percentage of positive outcomes and that no single clinical variable reliably predicted treatment results.117 Previous case series had indicated that SIJ RFN may have a role to play in the treatment of SIJ pain. The first main paper describing SIJ RFN used a stereotactic technique. After displaying the anatomy of the lateral branches of the sacral dorsal rami, Yin and associates reported in a retrospective audit that 64% of 14 patients treated with SIJ RFN reported successful outcomes for at least 6 months, with 36% achieving total relief.31 Kapural and coworkers performed a retrospective chart review on their initial cases using the cooled RFN technique; short term efficacy was apparent as 18 out of 26 cases had good outcomes at 3 months.118 They also performed a safety audit on the first 100 cases. There were no significant complications other than short-term (less than 6 weeks) pain exacerbation in four cases, and in two cases an area of cutaneous numbness over the buttocks was experienced.118 Mitchell and colleagues performed a prospective consecutive case series on 82 cases using a traditional RFN method directed at the L4 medial branch, the L5 dorsal ramus, and the S1-3 lateral branches.11 The cases were divided equally into 5- to 7-month and 8- to 13-month follow-up. Greater than 50% pain relief was

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achieved in 22% of patients in the 5- to 7-month group and 42% of patients in the 8- to 13-month group. Patient satisfaction was 58% versus 63% in the respective groups. At 8 months, the average reduction in VAS was 33%, with the 42% of patients with greater than 50% relief reporting an average reduction of 74% in VAS.112 Outcomes from treating the SIJ complex with traditional RF needles are dependent to some degree on the cause of the original injury; patients able to identify the cause of their injury (whether it be from a motor vehicle accident, fall, overload/work injury, etc.) are more likely to report excellent pain relief following RFN than those unable to pinpoint the mode of injury.82 Although sacral RFN is a safe procedure, there has been a case report of a permanent L5 sensory radiculopathy following a bilateral L3 to L5 RFN.119 However, such a complication should only arise from inaccurate positioning of the needle. Prolotherapy Prolotherapy for LBP including SIJ region pain and tenderness appears to be no better than placebo. In a RCT, Yelland and colleagues tested patients with LBP that might have included putative SIJ pain with injection onto any local tender structure—either with a combination of 20% glucose and 0.2% lidocaine or with saline.120 The outcome was that prolotherapy was equally effective as placebo but that both seemed to be somewhat effective (in 46% of cases there was a 50% pain reduction and in 42% of cases there was a 50% reduction) in Roland-Morris disability index. In a descriptive prospective trial case-series study, Cusi and associates examined functional outcome measures and improvements in load transfer on clinical examination but not pain after CT-guided injections of 50% glucose on three occasions 6 weeks apart.100 Functional improvement occurred in 76% of patients at 3- and 12-month follow-up and in 32% at 24-month follow-up. Surgery Surgery with SIJ arthrodesis (via a modified Smith-Petersen technique) for putative SIJ pain, diagnosed by pain relief with intraarticular joint injections under fluoroscopic guidance, has been studied and found in one series to be reasonably successful in terms of physical functioning, role physical, bodily pain, vitality, social functioning, role emotional, and neurogenic and pain indices.121 A caseseries on 15 consecutive patients treated with percutaneous SIJ fusion using hollow modular anchorage screws filled with demineralized bone matrix after diagnosis with a single SIJ injection of local anesthetic and steroid under image intensifier control reported that at a mean follow-up of 17 months, there was a significant improvement in disability, physical function, and pain; of the 15 patients, 13 reported good-to-excellent improvement.122 However, a more sobering picture emerges from a retrospective study on 17 patients who underwent bilateral SIJ fusion with internal fixation and decortication of the SIJ after diagnosis via local anesthetic joint infiltration, temporary external fixation, or bone scan because at an average follow-up period of 39 months only three patients (18%) reported moderate or absent pain; the rest of the patients had either marked or severe pain.123 Another much less invasive technique, SIJ débridement, was retrospectively studied on 38 patients with SIJ pain diagnosed with SIJ injection; at a follow-up period of 2 years, 61% had 50% or more reduction in pain and 53% had 75% or more reduction in pain.33 Additionally, percutaneous, CT-guided stabilization from S1-2, has been reported to be a potentially acceptable treatment for recalcitrant SIJ pain.124

Neuromodulation Neuromodulation with spinal cord stimulation, peripheral nerve stimulation,125 or sacral nerve stimulation can potentially relieve persistent pain from the SIJ that is recalcitrant to other therapies.

Methods Sacroiliac Joint Injection SIJ injection is perhaps the most difficult joint injection to perform because of the intricacies of SIJ morphology. It is generally easier to perform in the younger female in whom the joint space is likely to be wider. It can be difficult to perform in older people as the joint undergoes degeneration. It is not possible to inject into the joint when there it total ankylosis, but total bony ankylosis is seen only with ankylosing spondylitis.43 It can be difficult to get a synovial arthrogram in elderly men in particular because of the increasing age-related presence of complete fibrous SIJ ankylosis.42 If the injection is a diagnostic procedure, it is essential that a thorough pretest pain history is elicited, with the different areas of pain noted and the VAS in each of these areas recorded. It is also essential that the pain chart is again explained to the patient in recovery. The use of sedation prior to diagnostic procedures such as SIJ injection is dependent on clinician and patient preference. However, it is generally not required for SIJ injection unless the patient is needle phobic or pain sensitized. The patient lies prone on the x-ray table. Routine prepping and draping should occur and sterile technique is used throughout. The C-arm fluoroscope is centered over the inferior aspect of the appropriate SIJ. The object is to superimpose the dorsal and ventral joint lines at the inferior pole, so that a “clear” window is seen. It seems that no two joint lines are similar; thus, individual patient SIJ idiosyncrasies need to be recognized. One approach is to angle the C-arm between 10 and 20 degrees cephalic and, if the joint lines still do not overlap, to then vary the obliquity one way or the other by 5 and 10 degrees. If the joint lines still do not overlap, then repeat the same change of obliquity but with a caudad 10-to 20-degree tilt (Fig. 37-5). When the joint lines overlap, then a “down beam” approach to the inferior aspect of the joint line is performed with a 22 gauge spinal needle. The needle can be bent a few degrees, using a notouch technique, to allow the needle to be steered. Skin anesthesia is unnecessary. If the joint line is very sensitive on needle approximation, then 1 mL 2% lidocaine can be infiltrated at this point. However, for the purity of the block, it is preferable to not place local anesthetic outside the joint (Fig. 37-6). Resistance to the needle is felt as the joint capsule is entered, and often a “pop” is felt as the needle passes through the joint capsule; however, this is not a reliable sign of joint entry. When it is considered that the needle is intraarticular, the joint lines are separated radiologically by altering the obliquity back to a more PA tilt. The needle tip should still appear to be in one of the joint lines (Fig.  37-7). The C-arm is then adjusted obliquely the other way; again, the needle tip should appear to be in a joint line (Fig. 37-8). If this is not the case, contrast should NOT be injected. The needle is NOT in the joint and the approach view will be compromised if contrast is injected. If one of the oblique views does not show the needle in the joint, return to the approach view and insert the needle a further 2 mm or so. If doubt about the depth of the needle exists, use a lateral C-arm view for further assessment. Although the lateral view cannot confirm that the needle is

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Figure 37-5  SIJ injection AP view. Anteroposterior (AP) view with slight cephalic tilt showing the inferior aspect of the sacroiliac joint (SIJ) with ­ventral and dorsal joint lines overlapping. The implantable pulse generator from a spinal cord system is visible, as is the metal work from a previous posterior lumbar interbody fusion.

Figure 37-7  Sacroiliac joint (SIJ) injection needle—oblique needle view (right). The C-arm fluoroscopy is “obliqued” slightly to the patient’s right, showing that the needle tip is still in the joint line.

Figure 37-6  Sacroiliac joint (SIJ) injection—needle approach. The needle approaches the joint line “down beam” and is then slid superiorly into the joint.

Figure 37-8  Sacroiliac joint (SIJ) injection needle—oblique needle view (left). The C-arm fluoroscopy is “obliqued” to the patient’s left. The needle tip is still in a joint line.

intraarticular, it can ascertain whether or not the needle tip is a long way short of or past the joint. If both oblique views confirm the needle tip lies in one of the joint lines, then 0.2 mL of nonionic contrast is injected and then imaged. Contrast should flow into the joint with a minimum of resistance (Fig. 37-9). If resistance is encountered, then the needle is likely to be too ventral (too far into the joint). It can be carefully moved dorsally while maintaining pressure on the syringe; once the resistance lessens, contrast is then injected. If this dorsal movement is excessive, then the needle tip may become extraarticular; this component of needle tip positioning has to be extremely subtle. When the joint line is outlined adequately, the syringes are changed and formal joint injection is performed. It is essential to be assiduous in not moving the needle tip during the syringe exchange.

If the contrast is clearly not intraarticular, the whole process must be recommenced. If contrast obscures the views it may be propitious to abandon the procedure on that day. Occasionally it is not clear if the contrast is intra- or extraarticular; if this is the case, judicious injection of small aliquots of more contrast is reasonable. This injection should not be painful. However, if it is performed with more than minimal resistance, it is a painful procedure, and if so, it may be wise to warn the patient of this possibility. The deep interosseous ligament (DIL) can also be injected if there is a requirement to learn if this component is painful (by performing a diagnostic block) and/or to inject corticosteroid. The approach to the DIL is with the C-arm in a neutral cephalocaudad angle with contralateral oblique of 15 to 25 degrees. A “down beam” approach to touch the sacrum 1 cm medial to the DIL is used. The needle is then withdrawn 1 cm and “kicked” laterally into the DIL. The depth

Sacroiliac Joint Pain: Procedures for Diagnosis and Treatment  399

Figure 37-9  Sacroiliac joint (SIJ) injection needle—contrast flow. With needle placement confirmed, 0.2mL of contrast can now be confidently injected. Contrast is shown outlining the synovial part of the SIJ.

is level with the dorsal surface of the sacrum, up to a few mm superficial to the dorsal sacral boarder. Then 0.2 mL of nonionic contrast is injected to ensure the needle is not intravascular. The contrast should have a frothy or cloudlike appearance. If a striated pattern is seen, the needle is usually too ventral and is in the muscle ventral to the joint. If the contrast appears as a “blob” it is likely that the needle tip is too superficial. If in doubt, a lateral view may be helpful. There is no consensus on what medications to inject into the SIJ or DIL. If the injection is part of diagnostic series short- and long-acting local anesthetic agents are compared at different sessions. If particulate steroids are used, it is essential to ensure that the material is not injected intravascularly. Radiofrequency Neurotomy Controversy exists around the nerve supply to the SIJ complex, with nerves from the L3 medial branch to the S4 lateral branch all being implicated. Most published studies treat as cephalad as the L4 medial branch or the L5 dorsal branch; all studies treat down to S3. There are four techniques being espoused for performing a radiofrequency neurotomy of the SIJ complex: 1. Multiple lesions using traditional RFN needles around the inferolateral edges of S1-3, normal RF lesions on the L4 medial branch and L5 dorsal branch and a more lateral branch on the sacral ala to capture the L5 lateral branch. 2. Cooled RFN. This technique uses a patented technology to cool the tip of the RF probe with ice water to allow for a much bigger spherical lesion. These lesions are performed at 1:30, 3:00, and 4:30 (clock) positions on the right S1-3 foramen, and at 10:30, 9:00, and 7:30 on the left S1-3 foramen. 3. Simplicity technique. This patented technology involves placing a probe lateral to the sacral foramen from superior to S1 to inferior to S3. The probe then heats a 1 cm channel over a 7.5 ­minute cycle. L5 still needs to be treated in the traditional manner. 4. Pulsed RFN. This technique has been proved NOT to work on the spinal ZJs and there is no evidence for its efficacy in the management of SIJ pain.126

The first three of these techniques involve targeting the lateral branches from S1-3, as well as targeting L5 dorsal ramus and possibly the L4 medial branch. Therefore, knowledge of the nerve supply of the SIJ, and its variability, is essential. This includes the knowledge that the sacral lateral branches do not necessarily lie on bone as they leave the foramen; indeed they may lie up to 1 cm dorsal to the sacral surface. Both cooled RFN and the simplicity probe heat a large area seemingly enough to capture the variable nerve anatomy in the sacral region. Traditional RFN with a 16 gauge needle does not cover a 1 cm area, and it is a requirement that this technique is adjusted to treat all possible nerve pathways. Sometimes the anatomy of the sacrum and in particular the position of the sacral foramina can be difficult to visualize because of underlying bowel shadows. Hence, some clinicians prefer to recommend bowel prep the night prior to the procedure to remove feces and flatus underlying the sacrum. These procedures can be performed under sedation and/or with generous local anesthetic infiltration. Routine prepping and draping is performed. Traditional Method Normal RFN needles create a heat lesion in the axis of the exposed tip that has a radius three times the radius of the needle. The lesion extends approximately one needle width around the needle. The thicker the needle, the bigger the lesion that is created. Sixteen gauge needles are now available and should be used. The lesion does not extend beyond the tip of the needle. Thus, the RFN needle needs to be placed parallel to and in close contact with the nerves to be targeted. The C-arm is positioned PA with enough cephalic tilt to crisp the L5-S1 disc space. The S1-3 foramen should be visible with this approach. It is important to determine the site of the dorsal component of the sacral foramina; this may require movement of the C-arm in both oblique directions. Another way to localize the dorsal component of a sacral foramen is to insert a needle just into it by “walking” it from the adjacent posterior sacrum. Multiple lesions need to be performed at each level and the procedure is much more efficient if multiple needles are used at the same time. When all needles have been placed, the C-arm is swung to a lateral position. Care should be taken that the iliopectineal lines overlap (indicating the view is truly lateral relative to the pelvis). In this lateral view, the final needle adjustments are made. The L5 dorsal branch needle should not project beyond the superior edge of the sacral ala. The S1-3 needles should be seen to be lying flat on, or within 5 mm of, the dorsal surface of the sacrum and not inside a foramen. A further injection of 2% lidocaine is then injected down each needle. At this point, the first lesion is performed on all needles at 90° C for 90 seconds. A series of lesions around the inferolateral corner to the supero­ lateral corner of the S1-3 foramen should be performed. Each lesion should be less than 2 needle widths from the previous one. The area to be lesioned should cover all potential courses of the lateral branches (see Fig. 37-3). A second series of lesions should be performed 5 to 10 mm off bone to capture those nerves not lying on the sacral surface. The full course of the L5 dorsal branch needs to be covered. In addition to the lesion approaching the superior edge of the sacral ala, a pull back lesion should be performed. Additionally, a wide lesion, at least 5 mm lateral to the S1 superior articular process needs to be performed to cover the course of the L5 descending branch. An injection of cortisone at the conclusion of

37

400  Spine

Figure 37-10  Radiofrequency neurotomy (RFN)—anteroposterior (AP) view L4-S1. AP image with cephalic tilt showing needle on the L4 medial branch, L5 dorsal ramus, and S1 lateral branch.

Figure 37-12  Radiofrequency neurotomy (RFN)—anteroposterior (AP) view S1-3. (1) AP cephalic view showing RFN needles lateral to S1 foramen, inferolateral to S1 foramen, and lateral to S3 foramen. A needle performing an SIJ injection for postoperative pain relief is also shown.

Figure 37-11  Radiofrequency neurotomy (RFN)—lateral view L4-S1. Lateral image of L4 medial branch, L5 dorsal branch, and S1 lateral branch RFN. It is essential that this is true lateral. The iliopectineal lines must overlay (pelvis true lateral) and the iliac crests and L5 superior articular process must not be offset in a vertical direction (wig-wag).

Figure 37-13  Radiofrequency neurotomy (RFN)—anteroposterior (AP) view S1-3 contralateral approach. AP cephalic image showing RFN needles (placed from opposite side) 5 mm off bone at the inferolateral corners of the S1, S2, and S3 foramina.

the procedure over the areas treated may help with postoperative pain control (Figs. 37-10 to 37-13).

over the sacral foramen. The lesions are performed at least 1 cm from the lateral edge of each sacral foramen (Figs. 37-15 and 37-16).

Cooled Radiofrequency Neurotomy This technique involves the use of a trochar to introduce a cooled radiofrequency probe onto the lateral branches of S1, S2, and S3. A traditional RFN treatment of L5 is then performed. On the right side, the S1 and S2 lesions are performed at the 1:30, 3:00, and 5:30 clock positions; the S3 lesions at 3:00 and 5:00 o’clock positions. On the left side the lesions performed are obviously mirror imaged; the S1 and S2 lesions are performed at 10:30, 9:00, and 6:30 clock positions and the S3 lesions at the 9 and 7 o’clock positions (Fig. 37-14). The lesions are performed off the bony surface of the dorsum of the sacrum by use of a depth indicator with the position being guided by a radio-opaque “epsilon” that is positioned on the skin surface

Simplicity Radiofrequency Neurotomy There is currently no published outcome data on this technique, although the face validity of the technique is enticing. The technique involves placing the simplicity probe from a caudad direction under fluoroscopic control onto the dorsal surface of the sacrum lateral to the lateral edge of the sacral foramen. The probe has five different radiofrequency generators that sequentially perform RF lesions of approximately 5 mm radius along the length of the probe. The L5 branch needs to be treated separately with a traditional technique (Figs. 37-17 and 37-18).The technique is attractive with its ease of use and the size of the lesion developed. Outcome data are awaited.

Sacroiliac Joint Pain: Procedures for Diagnosis and Treatment  401

37

S1

S2

S3

Figure 37-16  Cooled radiofrequency neurotomy (RFN)—lateral view. ­ Lateral view of sacrum showing SInergy probe on S2 foramen. Figure 37-14  Cooled radiofrequency neurotomy (RFN) needle positions. On the right side, the S1 and S2 lesions are performed as at 1:30, 3:00, and 5:30 clock positions and the S3 lesions at 3:00 and 5:00. On the left side, the lesions performed are obviously mirror imaged; the S1 and S2 lesions are performed at 10:30, 9:00, and 6:30 and the S3 lesions 9:00 and 7:00.

Figure 37-17  Simplicity radiofrequency neurotomy (RFN)—anteroposterior (AP) view. This image shows the simplicity probe lateral to the dorsal foramen with a traditional RFN needle over the L5 dorsal ramus. Figure 37-15  Cooled radiofrequency neurotomy (RFN)—anteroposterior (AP) S1-3. SInergy probe over 3 o’clock position on S1 foramen. Note guiding needles in S2 and S3 foramen and the marking epsilon taped to the skin with sterile Steri-strips.

Prolotherapy Prolotherapy is a procedure whereby noxious agents are injected to create scar tissue, with the view that this will stiffen, or help stabilize a painful joint/segment and thus decrease pain arising from that segment. Various agents have been used in the past, with pumice

stone and glucose being the most popular; 12.5% to 50% glucose has been used the most. As noted above, the study of Yelland and colleagues did not support prolotherapy for LBP, but the technique was not performed on patients with proven SIJ pain and the injections were not performed using imaging.120 Cusi and coworkers reported a case series based on injection of 50% glucose with local anesthetic into the DIL under fluoroscopic guidance.100 This technique needs further evaluation. It is a painful procedure and is best performed

402  Spine

Figure 37-20  Prolotherapy—Contrast spread. Contrast showing spread through deep interosseous ligament (DIL) without vascular spread, 50% glucose can now be injected. Figure 37-18  Simplicity radiofrequency neurotomy (RFN)—lateral view. A lateral image of the simplicity probe and traditional RFN needle at L5.

Figure 37-19  Prolotherapy—Needle placement. Prolotherapy needle in right deep interosseous ligament (DIL)—precontrast. Note position 1 cm below superior edge of sacrum.

Figure 37-21  Prolotherapy—first needle reposition. The needle has been repositioned 1 cm lower.

under sedation. Routine prepping and draping are first performed. The C-arm is lined up on the affected DIL in a neutral cephalocaudad but contralateral oblique position. The posterior ilium is then almost end on and there is a direct route down to the superior SIJ. A point 1 cm below and medial to the superolateral edge of the sacrum is selected and a 22 gauge 3.5-inch spinal needle is inserted “down the beam” to touch the superolateral edge of the sacrum (Fig. 37-19). A small amount of contrast is injected to ensure the needle is not intravascular; then, 1 mL of local anesthetic is injected followed by 1.5mLs of 50% (or mix the two in the one syringe) (Fig. 37-20). Using the same skin entry point, the needle is readjusted laterally so that the tip is first at the very lateral edge of the sacrum at the same height, and then it is moved more laterally to the medial edge of the iliac bone at the same height; the same injection is repeated at both sites.

The needle is then repositioned on the sacrum 1 cm below the original position 1 cm medial to the lateral edge of the sacrum and the three injections are repeated by moving the needle tip each time more laterally so that the third injection is again on the medial wall and the procedure is repeated at this level; 1 cm medial to the lateral edge, on the lateral edge, and on the medial wall of the iliac bone (Fig. 37-21). The needle is again repositioned 1 cm lower where it now lies on or close to the SIJ line, and second injection is performed (Fig. 37-22). Contrast should be used with each reposition to ensure the needle is not placed intravascularly or intrasynovially. The patient receives routine monitoring in recovery and is discharged after a 2 or 3 hours. The patient will need adequate postprocedural analgesic. The procedure is repeated twice at 6-week intervals.

Sacroiliac Joint Pain: Procedures for Diagnosis and Treatment  403

Figure 37-22  Prolotherapy—second needle reposition. The needle has been repositioned 1 cm lower.

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404  Spine   44. Brooke R. The Sacro-Iliac Joint. J Anat. 1924;58:299-305.   45. Sashin D. A critical analysis of the anatomy and the pathological changes of the sacroiliac joints. JBJS. 1930;12:891-910.   46. Taggart AJ, Desai SM, Iveson JM, Verow PW. Computerized tomography of the sacro-iliac joints in the diagnosis of sacro-iliitis. Br J Rheumatol. 1984;23:258-266.   47. Vleeming A, de Vries HJ, Mens JM, van Wingerden JP, et al. Possible role of the long dorsal sacroiliac ligament in women with peripartum pelvic pain. Acta Obstet Gynecol Scand. 2002;81:430-436.   48. Vleeming A, Volkers AC, Snijders CJ, Stoeckart R. Relation between form and function in the sacroiliac joint. Part II: Biomechanical aspects. Spine. 1990;15:133-136.   49. Buyruk HM, Snijders CJ, Vleeming A, et al. The measurements of sacroiliac joint stiffness with colour Doppler imaging: a study on healthy subjects. Eur J Radiol. 1995;21:117-121.   50. Mens JM, Vleeming A, Snijders CJ, et al. The active straight leg raising test and mobility of the pelvic joints. Eur Spine J. 1999;8:468-473.   51. Mens JM, Vleeming A, Snijders CJ, et al. Reliability and validity of the active straight leg raise test in posterior pelvic pain since pregnancy. Spine. 2001;26:1167-1171.   52. Mens JM, Vleeming A, Snijders CJ, et al. Validity of the active straight leg raise test for measuring disease severity in patients with posterior pelvic pain after pregnancy. Spine. 2002;27:196-200.   53. Mooney V, Pozos R, Vleeming A, et al. Exercise treatment for sacroiliac pain. Orthopedics. 2001;24:29-32.   54. Sturesson B, Uden A, Vleeming A. A radiostereometric analysis of movements of the sacroiliac joints during the standing hip flexion test. Spine. 2000;25:364-368.   55. van Wingerden JP, Vleeming A, Buyruk HM, Raissadat K. Stabilization of the sacroiliac joint in vivo: verification of muscular contribution to force closure of the pelvis. Eur Spine J. 2004;13:199-205.   56. van Wingerden JP, Vleeming A, Ronchetti I. Differences in standing and forward bending in women with chronic low back or pelvic girdle pain: indications for physical compensation strategies. Spine. 2008;33:E334-E341.   57. Grob KR, Neuhuber WL, Kissling RO. Innervation of the sacroiliac joint of the human. Z Rheumatol. 1995;54:117-122.   58. Dreyfuss P, Henning T, Malladi N, et al. The ability of multi-site, multi-depth sacral lateral branch blocks to anesthetize the sacroiliac joint complex. Pain Med. 2009;10:679-688.   59. Willard FH, Carreiro JE, Manko W: The long posterior interosseous ligament and the sacrcoccygeal plexus. Third Interdisciplinary World Congress on Low Back and Pelvic Pain. Proceedings of the Third Interdisciplinary World Congress on Low Back and Pelvic Pain, 207–209.   60. Dreyfuss P, Snyder BD, Park K, et al. The ability of single site, single depth sacral lateral branch blocks to anesthetize the sacroiliac joint complex. Pain Med. 2008;9:844-850.   61. Hides JA, Jull GA, Richardson CA. Long-term effects of specific stabilizing exercises for first-episode low back pain. Spine. 2001;26:E243-E248.   62. Hides JA, Richardson CA, Jull GA. Multifidus muscle recovery is not automatic after resolution of acute, first-episode low back pain. Spine. 1996;21:2763-2769.   63. Richardson CA, Snijders CJ, Hides JA, et al. The relation between the transversus abdominis muscles, sacroiliac joint mechanics, and low back pain. Spine. 2002;27:399-405.   64. Hodges P, Jull G. Does strengthening the abdominal muscles prevent low back pain? J Rheumatol. 2000;27:2286-2288.   65. Jull GA, Richardson CA. Motor control problems in patients with spinal pain: a new direction for therapeutic exercise. J Manipulative Physiol Ther. 2000;23:115-117.   66. Sapsford RR, Hodges PW, Richardson CA, et al. Co-activation of the abdominal and pelvic floor muscles during voluntary exercises. Neurourol Urodyn. 2001;20:31-42.   67. Sterling M, Jull G, Wright A. The effect of musculoskeletal pain on motor activity and control. J Pain. 2001;2:135-145.

  68. Cattley P, Winyard J, Trevaskis J, Eaton S. Validity and reliability of clinical tests for the sacroiliac joint. A review of literature. Australas Chiropr Osteopathy. 2002;10:73-80.   69. Damen L, Buyruk HM, Guler-Uysal F, et al. The prognostic value of asymmetric laxity of the sacroiliac joints in pregnancy-related pelvic pain. Spine. 2002;27:2820-2824.   70. Damen L, Spoor CW, Snijders CJ, et al. Does a pelvic belt influence sacroiliac joint laxity? Clin Biomech. 2002;17:495-498.   71. Damen L, Stijnen T, Roebroeck ME, et al. Reliability of sacroiliac joint laxity measurement with Doppler imaging of vibrations. Ultrasound Med Biol. 2002;28:407-414.   72. Damen L, Buyruk HM, Guler-Uysal F, et al. Pelvic pain during pregnancy is associated with asymmetric laxity of the sacroiliac joints. Acta Obstet Gynecol Scand. 2001;80:1019-1024.   73. Mens JM, Damen L, Snijders CJ, et al. The mechanical effect of a pelvic belt in patients with pregnancy-related pelvic pain. Clin Biomech. 2006;21:122-127.   74. Coventry MB, Tapper EM. Pelvic instability: a consequence of removing iliac bone for grafting. J Bone Joint Surg Am. 1972;54:83-101.   75. Elgafy H, Semaan HB, Ebraheim NA, Coombs RJ. Computed tomography findings in patients with sacroiliac pain. Clin Orthop Relat Res. 2001:112-118.   76. Summers BN, Eisenstein SM. Donor site pain from the ilium. A complication of lumbar spine fusion. J Bone Joint Surg Br. 1989;71:677-680.   77. Ebraheim NA, Elgafy H, Semaan HB. Computed tomographic findings in patients with persistent sacroiliac pain after posterior iliac graft harvesting. Spine. 2000;25:2047-2051.   78. Maigne JY, Planchon CA. Sacroiliac joint pain after lumbar fusion. A study with anesthetic blocks. Eur Spine J. 2005;14:654-658.   79. Ivanov AA, Kiapour A, Ebraheim NA, Goel V. Lumbar fusion leads to increases in angular motion and stress across sacroiliac joint: a finite element study. Spine. 2009;34:E162-E169.   80. Ha KY, Lee JS, Kim KW. Degeneration of sacroiliac joint after instrumented lumbar or lumbosacral fusion: a prospective cohort study over five-year follow-up. Spine. 2008;33:1192-1198.   81. Tuite MJ. Sacroiliac joint imaging. Semin Musculoskelet Radiol. 2008;12:72-82.   82. Mitchell B, McPhail T, Verrills P, et al. Chronic pelvic and sacroiliac joint pain: Diagnosis, radiofrequency neurotomy and neuromodulation. APS/NZPS Combined Conference. 2010.   83. Szadek KM, van der WP, van Tulder MW, et al. Diagnostic validity of criteria for sacroiliac joint pain: a systematic review. J Pain. 2009;10:354-368.   84. Feinstein B, Langton JN, Jameson RM, Schiller F. Experiments on pain referred from deep somatic tissues. J Bone Joint Surg Am. 1954;36-A:981-997.   85. Govind J. Lumbar radicular pain. Aust Fam Physician. 2004;33:409-412.   86. Irwin RW, Harris MB. Concomitant sacroiliac joint pain in patients with lumbar disc herniation: case series. J Surg Orthop Adv. 2004;13:224-227.   87. Kutsy RL, Robinson LR, Routt Jr ML. Lumbosacral plexopathy in pelvic trauma. Muscle Nerve. 2000;23:1757-1760.   88. Dreyfuss P, Michaelsen M, Pauza K, et al. The value of medical history and physical examination in diagnosing sacroiliac joint pain. Spine. 1996;21:2594-2602.   89. Berthelot JM, Labat JJ, Le Goff B, et al. Provocative sacroiliac joint maneuvers and sacroiliac joint block are unreliable for diagnosing sacroiliac joint pain. Joint Bone Spine. 2006;73:17-23.   90. Laslett M, Williams M. The reliability of selected pain provocation tests for sacroiliac joint pathology. Spine. 1994;19:1243-1249.   91. Laslett M. The value of the physical examination in diagnosis of painful sacroiliac joint pathologies. Spine. 1998;23:962-964.   92. Laslett M. Pain provocation tests for diagnosis of sacroiliac joint pain. Aust J Physiother. 2006;52:229.   93. Laslett M. Evidence-based diagnosis and treatment of the painful sacroiliac joint. J Man Manip Ther. 2008;16:142-152.

Sacroiliac Joint Pain: Procedures for Diagnosis and Treatment  405   94. Laslett M, Aprill CN, McDonald B, Young SB. Diagnosis of sacroiliac joint pain: validity of individual provocation tests and composites of tests. Man Ther. 2005;10:207-218.   95. Laslett M, Aprill CN, McDonald B. Provocation sacroiliac joint tests have validity in the diagnosis of sacroiliac joint pain. Arch Phys Med Rehabil. 2006;87:874-875.   96. Dreyfuss P, Dryer S, Griffin J, et al. Positive sacroiliac screening tests in asymptomatic adults. Spine. 1994;19:1138-1143.   97. Hungerford B, Gilleard W, Hodges P. Evidence of altered lumbopelvic muscle recruitment in the presence of sacroiliac joint pain. Spine. 2003;28:1593-1600.   98. Hungerford B, Gilleard W, Lee D. Altered patterns of pelvic bone motion determined in subjects with posterior pelvic pain using skin markers. Clin Biomech. 2004;19:456-464.   99. Hungerford BA, Gilleard W, Moran M, et al. Evaluation of the ability of physical therapists to palpate intrapelvic motion with the Stork test on the support side. PhysTher. 2007;87:879-887. 100. Cusi M, Saunders J, Hungerford B, et al. The use of prolotherapy in the sacroiliac joint. Br J Sports Med. 2010;44:100-104. 101. Buyruk HM, Stam HJ, Snijders CJ, et al. The use of color Doppler imaging for the assessment of sacroiliac joint stiffness: a study on embalmed human pelvises. Eur J Radiol. 1995;21:112-116. 102. Weil YA, Hierholzer C, Sama D, et al. Management of persistent postpartum pelvic pain. Am J Orthop. 2008;37:621-626. 103. Prassopoulos PK, Faflia CP, Voloudaki AE, Gourtsoyiannis NC. ­Sacroiliac joints: anatomical variants on CT. J Comput Assist Tomogr. 1999;23:323-327. 104. Slipman CW, Sterenfeld EB, Chou LH, et al. The value of radionuclide imaging in the diagnosis of sacroiliac joint syndrome. Spine. 1996;21:2251-2254. 105. Faflia CP, Prassopoulos PK, Daskalogiannaki ME, Gourtsoyiannis NC. Variation in the appearance of the normal sacroiliac joint on pelvic CT. Clin Radiol. 1998;53:742-746. 106. Klauser AS, De Zordo T, Feuchtner GM, et al. Fusion of real-time US with CT images to guide sacroiliac joint injection in vitro and in vivo. Radiology. 2010;256(2):547-553. 107. Streitparth F, Walter T, Wonneberger U, et al. Image-guided spinal injection procedures in open high-field MRI with vertical field orientation: feasibility and technical features. Eur Radiol. 2010;20: 395-403. 108. Lord SM, Barnsley L, Bogduk N. The utility of comparative local anesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical zygapophysial joint pain. Clin J Pain. 1995;11:208-213. 109. Schwarzer AC, Aprill CN, Derby R, et al. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophysial joints. Pain. 1994;58:195-200. 110. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine. 1996;21:1889-1892.

111. Manchikanti L, Singh V, Pampati V, et al. Evaluation of the relative contributions of various structures in chronic low back pain. Pain ­Physician. 2001;4:308-316. 112. Mitchell B, McPhail T, Verrills P, et al. Radiofrequency neurotomy for sacroiliac joint pain: A prospective study. J Science Med Sport. 2010;12(Supp 2):e6-e7. 113. Hawkins J, Schofferman J. Serial therapeutic sacroiliac joint injections: a practice audit. Pain Med. 2009;10:850-853. 114. Cui Y, Xiao Z, Shuxia W, et al. Computed tomography guided intraarticular injection of etanercept in the sacroiliac joint is an effective mode of treatment of ankylosing spondylitis. Scand J Rheumatol. 2010;39:229-322. 115. Cohen SP, Hurley RW, Buckenmaier III CC, et al. Randomized ­placebo-controlled study evaluating lateral branch radiofrequency denervation for sacroiliac joint pain. Anesthesiology. 2008;109:279-288. 116. Cohen SP, Raja SN: A placebo-controlled study assessing lateral branch radiofrequency denervation for sacroiliac (SI) joint pain. 2008. Unpublished Work 117. Cohen SP, Strassels SA, Kurihara C, et al. Outcome predictors for sacroiliac joint (lateral branch) radiofrequency denervation. Reg Anesth Pain Med. 2009;34:206-214. 118. Kapural L, Stojanovic M, Bensitel T, et al. Cooled radiofrequency (RF) of L5 dorsal ramus for RF denervation of the sacroiliac joint: technical report. Pain Med. 2010;11:53-57. 119. Abbott Z, Smuck M, Haig A, Sagher O. Irreversible spinal nerve injury from dorsal ramus radiofrequency neurotomy: a case report. Arch Phys Med Rehabil. 2007;88:1350-1352. 120. Yelland MJ, Glasziou PP, Bogduk N, et al. Prolotherapy injections, saline injections, and exercises for chronic low-back pain: a randomized trial. Spine. 2004;29:9-16. 121. Buchowski JM, Kebaish KM, Sinkov V, et al. Functional and radiographic outcome of sacroiliac arthrodesis for the disorders of the sacroiliac joint. Spine J. 2005;5:520-529. 122. Khurana A, Guha AR, Mohanty K, Ahuja S. Percutaneous fusion of the sacroiliac joint with hollow modular anchorage screws: clinical and radiological outcome. J Bone Joint Surg Br. 2009;91:627-631. 123. Schutz U, Grob D. Poor outcome following bilateral sacroiliac joint fusion for degenerative sacroiliac joint syndrome. Acta Orthop Belg. 2006;72:296-308. 124. Ziran BH, Heckman D, Smith WR. CT-guided stabilization for chronic sacroiliac pain: a preliminary report. J Trauma. 2007;63:90-96. 125. Verrills P, Mitchell B, Vivian D, Sinclair C. Peripheral nerve stimulation: A treatment in chronic low back pain and failed back surgery syndrome? Neuromodulation. 2009;12:68-75. 126. Tekin I, Mirzai H, Ok G, et al. A comparison of conventional and pulsed radiofrequency denervation in the treatment of chronic facet joint pain. Clin J Pain. 2007;23:524-529.

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38

Discography David G. Vivian, MM, BS, FAFMM, and Milton H. Landers, DO, PhD PART A THEORETICAL ASPECTS David G. Vivian, MM, BS, FAFMM

Discography is used to determine if an intervertebral disc is the likely source of pain in a person presenting with referred pain thought to derive from an innervated spinal structure. If positive, it leads either to a target-specific treatment or to cessation of the search for the source of the pain. However, its methodology and usefulness as a predictor of successful target-specific treatment remain contentious. The superiority of discography over other imaging methods to demonstrate morphology is not disputed. However, this advantage is of no particular use because morphologic change is nonspecific. Disc degeneration (DD) as determined by discography, magnetic resonance imaging IMRI), and other imaging tests occurs with similar frequency in symptomatic and asymptomatic populations. The controversy about discography relates mainly to its subjective component. During discography, attempts are made to reproduce or relieve the patient’s pain. Researchers, cognizant of the inaccuracies of discography, continue to refine this component; future developments may focus on whether or not analgesic discography (AD) and functional analgesic discography (FAD) add to its validity. There are four important aspects to the concept of discography that should be implicitly understood (Table 38-1). First, although there are substantial clinicopathologic correlates in the lumbar spine, it does not define a specific pathologic process that might have rendered the disc painful. It is, in particular, a procedural test that attempts to identify a cohort of otherwise labeled nonspecific spinal pain (NSSP) patients with a particular type of discogenic pain (DP), called internal disc disruption (IDD). Second, in IDD there is no breach of the outer annulus fibrosus (AF); thus, when the disc is pressurized for the subjective part of the discogram, it is possible to reproduce the patient’s pain in the case of provocation discography (PD) and reduce pain in the case of AD, as the injected material is confined to the disc. Third, discography cannot identify patients with putative DP in whom there is a breach of the external border of the AF, as consequent leakage of injected material is prone to both false-negative results (the pressure is insufficient to propagate intradiscal nociception or local anesthetic concentrations are insufficient to block nociception) and false-positive results (due to anesthetization subsequent to epidural spread of the local anesthetic). Fourth, there is no definitively proven treatment that has arisen for patients with IDD.

History and Development of Discography After 1934, when Mixter and Barr published on disc prolapse and neural compression,1 most back pain was thought to arise from disc prolapse, yet it became apparent that neural compression was found only in a relatively small number of patients with spinal pain. Furthermore, disc prolapse has been shown to be common in the asymptomatic population (for example, a prevalence of 37% in the thoracic spine).2 Discography, pioneered from 1947 by investigators such as Inman and Saunders,3 Falconer and colleagues4 and Wiberg,5 arose before the disc was considered or proven to be innervated and at the time when the cause of back pain and radicular pain was considered to be disc prolapse. The first clue to the possibility of intrinsic DP occurred when back pain was produced by probing the posterior AF during lumbar disc surgery performed under local anesthesia.6 Despite the prevailing view that the disc was aneural, various authors reported that there was a relationship between disc morphology and reproduction of back pain; and, more particularly, that morphologically normal discs were rarely painful, in contrast to degenerative discs with posterior bulges and discs with epidural leaks on discography which were virtually always painful.7,8 Researchers then attempted to determine if abnormal discs occurred in patients without pain. Massie and Stevens, who reported their findings on discography in 52 normal subjects and 570 patients, found that abnormal discs were associated with age and far more common in patients with pain than in asymptomatic controls, and that in asymptomatic subjects, abnormal discs were rarely painful on PD.9 After this PD fell into disrepute when Holt reported a false-positive rate of 37% in a group of asymptomatic prisoners,10 but a later in-depth study refuted this report on methodologic grounds.11 Subsequent to this there was a period of debate about the role of discography, leading in 1988 to a position statement on discography by NASS that emphasized the pain-response as the most important part of the procedure,12 thereby restating the fact that abnormal morphology is of minimal relevance when the diagnostic methodology seeks to establish if the disc is the source of an individual’s pain. Then, using a more refined technique, Walsh and colleagues studied a selection of normal volunteers and patients with low 407

408  Spine

Table 38-1  Four Fundamental Concepts of Discography Discography is a quasi-subjective test that attempts to define the disc as a source of pain: it does not establish the pathophysiology of the pain. In internal disc disruption (IDD) there is, by definition, disruption of the normal internal disc architecture, often with radial or circumferential tears in the annulus fibrosis. Discography cannot identify patients with putative discogenic pain in whom there is a breach of the external border of the AF. There is no proven treatment that has arisen for patients with pain with IDD.

back pain.13 In this study, the discographer was blinded in all respects, and the patient responses were filmed and assessed by two external observers. This study revealed that normal discs in asymptomatic volunteers do not hurt, and only abnormal discs in patients are painful. At this time, therefore, PD performed in this manner was considered a highly specific procedure for symptomatic (painful) lumbar discs. The next development was the finding that axial view CT discography revealed radial dispersal of contrast medium in distinct patterns of radial and circumferential fissures in the AF.14,15 From this arose the Dallas discogram scale,16 later modified by Aprill and Bogduk,17 where Grade 0 describes contrast medium contained wholly within a regular NP, grades 1 to 3 describe extension of contrast medium along radial fissures into the inner third, middle third, and outer third of the AF, respectively, grade 4, in which grade 3 fissures extend circumferentially around the AF by at least 30 degrees of arc, and grade 5 in which the fissures breach the outer lamellae of the AF. The morphologic patterns of disc disruption and the innervation of these different areas lead to a consideration that there was a greater chance of the more peripheral fissures being painful. By this time it was established that the inner third of the AF is never innervated, the outer third is regularly innervated, and the middle third may or may not be innervated. Subsequently, Vanharanta and coworkers corroborated this clinicopathologic model by determining that on PD grade 0 and grade 1 disruptions are rarely painful, in contrast to grade 3 disruptions, which are associated with exact or similar pain reproduction in 75% of cases.18 Moneta reported that only grade 3 and 4 fissures reproduced pain that closely approximated the patient’s reporting of pain, and that annular fissures were not a feature of disc aging or degeneration.19 By the 1990s it was determined that for NSLBP there were firm correlations between the innervation of the disc, pain reproduction from it, and a demonstrable lesion, namely, IDD. Since then, a number of researches, particularly Carragee, have studied PD in depth. The first criticism leveled on PD is that it is nonspecific and fails because it produces excessive false-positive results.20-25 It should also be noted that use of pain provocation is questionable in other pain diagnosis areas, such as in the detection of zygapophysial joint pain.26 Studies that question the validity of PD include: Patients who prior to a bone graft procedure had no LBP, and who developed back or buttock pain after the procedure, were subjected to PD; in this series of 8 patients, 50% were considered to fulfil the criteria for IDD.25 ll In patients with persistent LBP after laminotomy and discectomy for disc prolapse, the relative pain intensity response to PD in these symptomatic subjects was compared to that of those who ll

were asymptomatic after the same operation. It was found that, independent of psychometric profiles, a high percentage (about 40%) of this asymptomatic group had a pain response equivalent to what would be considered positive pain provocation on PD; this contrasted to a 70% positive PD pain response in the symptomatic group. Additionally, in both groups, patients with abnormal psychologic profiles had significantly higher rates of positive disc injections than either asymptomatic volunteers or symptomatic subjects with normal psychological screening.23 ll Subjects without chronic LBP but with clinical profiles similar to those of symptomatic LBP subjects were investigated with PD. Of this group, 10 had no pain anywhere, 10 had chronic neck and arm pain, but no LBP; and 6 were considered to have “primary somatization disorders” without low back symptoms.34 Significant positive pain response and pain-related behavior were found in 10% of the pain-free group, in 40% of the chronic cervical pain group, and in 83% of the somatization disorder group completing the injections. Twenty-four subjects had negative control discs. It was concluded that the rate of false-positive discography is low in subjects with normal psychometric profiles and without chronic pain, but it is moderate in subjects with tears of the AF and chronic pain or abnormal psychometric testing. ll Subjects with NSLBP with disability and pain of insufficient degree for them to seek treatment for this symptom were subjected to PD, and the results were compared to a group with NSLBP being considered for surgery. In the control group 36% of subjects had a positive PD including the demonstration of AF disruption to or through to the outer AF and negative control discs. The comparison showed that more prominent NSLBP subjects were PD positive in 73% of cases.21 ll From a morphologic perspective, discography is not predictive, and moderate-to-severe Modic changes are weakly predictive, of future development of serious NSLBP in subjects with either mild persistent low back pain or some other mild pain symptom, whereas abnormal psychosocial risk factor profiles are predictive.22 As discussed earlier, the false-positive rates for PD in a carefully selected group are consid1ered to be 10%, but this figure increases to at least 25% in patients with abnormal psychologic profiles and in those with pain in other regions.

Discography as Criterion Standard Test In medicine, a primary aim is to make a diagnosis based on solid criteria that definitively establish if a specific disease or condition exists. The criteria that underpin a reliable diagnosis are measured by diagnostic tests. Examples of the best criterion standards include pathologic specimens to diagnose cancer and infection, imaging for bone disease and fracture and angiography to detect vascular disease. Certain standards have been iterated for rating the tests used to confirm a diagnosis.27-29 Some criterion standard tests are not routinely used because they are expensive, inaccessible, invasive, and risky.30 As a consequence, other diagnostic tests are used as surrogate criterion standard tests.30 Although surrogate tests might be cheaper, more available, less invasive, and safer; they might also be less accurate. Robust diagnosis is not possible in many areas of pain medicine, and especially in the diagnosis of NSSP, because of the lack of a good criterion standard test. In putative DP even tissue biopsy is unhelpful

Discography  409

Table 38-2  Diagnostic Criteria for Discogenic Pain Secondary to Internal Disc Disruption (IDD)* Patient’s pain is reproduced by stimulation of the affected disc. This pain must have an intensity of at least 7 on a 10-point scale. This pain must be reproduced at a low to intermediate pressure of ­stimulation: 15-30 psi above opening pressure (1-3 kg/cm2) Stimulation of adjacent disc(s) must not reproduce pain. Postdiscography CT must demonstrate a grade 3 or 4 fissure. *From International Spine Intervention Society (ISIS, 2004).31 All categories must be satisfied. These criteria are being modified.

in determining whether or not the disc is a source of pain. MRI may have a role in the detection of DP, but overall it has not been accepted as valid because it is not generally predictive of pain. Thus, in NSSP there is no criterion standard based on pathology, and no simple imaging test acting as an acceptable surrogate. Discography has been advocated as the best test, but it comes with costs of limited availability, some risks, limited reliability, and less than ideal validity. The diagnostic dilemma encountered where there is no reasonable criterion standard is overcome by using a classification system that is based not on pathology, but on a manifesting symptom. Notable examples of such well recognized classification systems predicated on symptoms rather than on robust criterion-based tests include the classification system for psychiatric disorders, called the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV),32 and the classification system for headache, called the International Classification of Headache Disorders (ICHD).33 DSM-IV is a categoric classification system for psychiatric diagnosis in which the categories are prototypes, and a patient with a close approximation to the prototype is said to have that disorder. The ICHD classifies all headache disorders into major groups and each group is then subdivided one, two, or three times into headache types, subtypes, and subforms. Migraine is a diagnosis in this system. There is no test that confirms the diagnosis. It is a symptom-based diagnosis which has subtypes of migraine such as “migraine with aura,” further subgrouped into subforms such as “typical aura with migraine headache.” The ICHD uses all kinds of available evidence (clinical description, longitudinal studies of cohorts of patients, epidemiologic studies, treatment results, genetics) to establish such a diagnostic entity. A diagnosis is required not only for individual patient management, but also so that diagnosis based management can be evaluated for all populations. Discography reveals the likely source of pain for some patients presenting with otherwise classified NSSP. It also provides a mechanism for the pain, namely IDD. The validity of the diagnosis IDD, and hence the assessment of treatment related to IDD, is predicated primarily on the validity of ­discography (Table 38-2).

The lumbar discs consist of a central NP surrounded by the AF which consists of concentric laminae of collagen fibers thickest anteriorly and laterally.34 In contrast, cervical discs consist of a crescent-shaped anterior interosseous ligament with thick anterior collagen fibers that taper laterally toward the uncinate processes; they are essentially deficient posterolaterally where there is only a thin layer of paramedian, vertically orientated fibers.35 The anterior longitudinal ligament covers the front of the cervical disc, and the posterior longitudinal ligament reinforces the deficient posterior AF with longitudinal and alar fibers.35 Cervical discs have a different chemical morphology to thoracic and lumbar discs. In particular, they contain a higher collagen content in the NP and higher glycosaminoglycans content in the AF, both of which allow for the greater demands of bending and twisting movements in the cervical spine compared to other spinal regions.36 Because discs are innervated, they have the capacity to be sources of pain.37 The normal disc is avascular and aneural except for the outer third of the AF.38,39 Lumbar discs are innervated by the lumbar sinuvertebral nerves, and branches of the lumbar ventral rami and grey rami comunicantes.40-42 There are five types of nerve terminations found in the lumbar disc: these have various morphologies and include simple and complex free nerve endings that concentrate particularly in the lateral disc, with a smaller amount posteriorly and the least amount anteriorly.43 The posterolateral portion of lumbar discs are innervated by the lumbar ventral rami that arise just lateral to the intervertebral foramen and by a branch of the grey rami communicans just before it connects with the ventral ramus.40 The sinuvertebral nerves also innervate the posterior longitudinal ligament, and the grey rami communicantes also innervate the lateral disc and the anterior longitudinal ligament.40,41 Additionally, the innervation by the grey rami communicantes is not a direct sympathetic innervation;40 it has been postulated that somatic and afferent fibers from lumbar structures use the grey rami as transmission pathways only.41 Cervical discs are innervated laterally by branches of the vertebral nerve and more generally by branches of the cervical sinuvertebral nerves; these nerves penetrate as deeply as the outer third of the AF.38,44 The end-plate adjacent to the NP is also innervated.45 In discogram positive discs, histologic studies have shown that there is there is a more extensive and deeper innervation of the disc, with free nerve endings expressing substance P reaching into the outer part of the NP,37,46,47 as well as the adjacent end plate and vertebral body.48 The ingrowth of nerves in the discogram positive disc is within a region of vascularized and innervated granulation tissue that accompanies fissures extending from the AF to the outer part of the NP.47 These nerves contain increased substance P (SP), neurofilament (NF), and vasointestinal peptide (VIP) immunoreac-tive nerve fibers, and are consistent with the concept of DP.47

Disc Degeneration

Disc Morphology Anatomy There is a gradual transition of disc morphology from the cervical spine, where movement is more relevant than loading, to the lower lumbar spine, where intervertebral movements are smaller, and load transfer is maximal.

Disc degeneration and similar morphologically descriptive terms including degenerative disc disease and zygapophysial joint spondylitis, are imaging-related labels that should not be used as diagnostic labels for a person presenting with NSSP. These terms describe mid- to late-stage degenerative change seen on imaging techniques. Although there may be a mild link between some imaging changes and NSSP,49 there is at present no reliable or valid method to detect this relationship in any individual case.50,51

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Degeneration is an inevitable process. The process of degeneration consists of gradual structural change, which at times is accompanied by altered homeostasis and changes in innervation. Although such a process might be painful in its own right, or might determine that the whole intervertebral segment is prone to pain, there does not appear to be an inevitability that pain will appear. Thus, DD can be observed, but at this stage of science, little if any pain attribution can be assigned to it. Put simply, DD is not DP! The IVDs are mainly composed of extracellular matrix molecules and have only about 1% by volume cell content, with the content of cells decreasing from the periphery inward, reflecting the relative avascularity of the disc.52 These cells are of vital importance for disc homeostasis because they regulate the synthesis and metabolism of the extracellular matrix. DD is represented at a molecular level by a relative rise in the quantity of senescent cell population on the background of an overall fall in the total number of cells within the disc.53 The percentage of senescent cells within a disc is also inversely related to the ability of other cells to proliferate, and the relative quantity of senescent and proliferating cells is independent of age.53 DD ends with structural failure, represented macroscopically by thickened vertebral end plates, increased cracks and fissures in the matrix, and delamination and tears in the AF.54 The radiologic endpoint of DD is disc space narrowing and osteophyte formation.54 Cellular function within the disc is mediated by at least five major factors: genetics, nutrition (diffusion of nutrients and oxygen across the disc matrix), cell function regulation via IL-1, TNF-α and TNF-β, age and senescence, and mechanical loading.55 The contribution to DD by genetic factors is highly significant; it may be as high as 80% in the cervical spine,56 and general heritability for DD ranges from 34% to 61% in different regions of the spine.57 In the lumbar spine, the genetic contribution is between 29% and 54%, with environmental influences of about equal importance.58 For example, smoking has a moderate influence on the prevalence of DD,59 presumably due to its effects on disc nutrition. This emphasizes that DD is not primarily or significantly due to aging60 or to mechanically induced “wear and tear” processes.57,61 Studies on symptomatic and asymptomatic populations with various imaging modalities emphasize that DD does not imply NSSP. In the cervical spine, radiologic DD is present in 13% of men and 5% of women during the third decade, in 85% to 90% of the population by the sixth decade, and nearly 100% by the age of 70.62 It occurs most commonly at C5-6, C6-7, and C4-5, respectively.63,64 In people aged 60 to 65 years without neck pain, about 95% of men and 70% of women have at least one degenerative change on their cervical spine plain x-rays.63 Although plain x-ray changes, including vertebral end-plate changes, disc space narrowing, spondylolisthesis, spondylolysis, sacral lumbarization, wedge vertebra, a sagittal diameter of less than 12 mm, and abnormal lumbar lordotic angle,49,65,66 have some predictive value for low back pain, the relationship is mild at best,67 and their detection is largely not helpful in the management of NSLBP because changes occur frequently in the asymptomatic population. As a consequence, plain x-rays should not be ordered unless there is suspicion of a red-flag condition.68-71 The relevance of computed tomography (CT) scanning is similar to plain x-rays; it is an excellent test for some red-flag conditions, demonstrates DD well, but it is not helpful in the detection of DP. CT is better than MRI in detecting ZJ spondylitis,72 but this is of no particular clinical relevance. F-PET/CT (fluoride positron emission tomography with addition of CT) may have a role to play in that it

is more likely to be positive in symptomatic patients, and in that it might identify the source of pain.73 Plain x-rays combined with MRI provide the best method to detect DD.74 Plain x-rays are perhaps better than MRI at detecting early stages of DD; MRI detects later stages of DD.74 However, such information is only relevant to research because the detection of DD does not help in the diagnosis of NSSP. Studies of asymptomatic subjects have shown degenerative rates of more than 30% in the general population.75 Discography is the best method to detect gross disc morphology. Fissures can be detected best on CT imaging postcontrast injection. However, although this component of discography detects degeneration, such a finding does not mean that the disc is a source of pain. For this reason, discography evolved from a purely morphologic test to one that attempts to detect whether or not the disc is painful. Discography, like other imaging modalities, should not be ordered in an effort to detect degeneration because degeneration is not a legitimate diagnosis for NSSP.

Discography and Pain The relative uselessness of morphologic changes in the search for a source of pain has lead to the search for the painful source using two mechanisms; pain provocation and pain reduction. Discography can theoretically cause pain from the disc itself by two fundamental mechanisms, annular distention and endplate deflection. Annular distention during discography can initiate nociception because the peripheral AF is innervated. In vitro study has shown that in radiographically nondegenerated discs, discography causes measurable end-plate deflection ranging from 0.12 to 0.69 mm centrally and from 0.06 to 0.35 mm at locations between the center and the periphery of the end plate.76 Hsu investigated 692 discs in patients with back pain; he showed that during PD end-plate disruption is uncommon (2% of all discograms) but that when it occurs even with lightly induced pressure, the prevalence of moderate or severe fully concordant pain is very high (in this series, 13/14 or 93%); in contrast, 42.3% of the remaining discs without end-plate disruption had moderate-to-severe fully concordant pain on PD, and 57.7% had either mild or zero pain.77 Pain reproduction during the disc stimulation component of PD is considered integral to its validity. All discs, if provoked enough, will produce pain. However, a study on asymptomatic subjects revealed that even if grade 3 annular tears are present, pain induced on PD is likely to be mild—even at high manometric pressures.78 From this study, pressures below which pain does not occur or it occurs at low intensity have been identified for asymptomatic subjects. The assumption is that this effect should be mirrored in studies of symptomatic patients, so that manometric pressure readings can be titrated against pain scores to set parameters above which the procedure can be called positive. For example, at a pressure of 50 psi any pain score above 6/10 is not seen in asympto­matic volunteers: at a pressure of 40 psi, the cutoff score is 5/10. Put another way, there is close to zero chance of an asymptomatic subject having any pain at 20 psi or less, and of having pain greater than 6/10 up to a pressure of 70 psi.79 When the criterion for a positive PD pain response is 6/10 or more at 50 psi, the false-positive rates in asymptomatic subjects falls to 10%.79 Derby and colleagues then found that there was a correlation between postdiscography CT scan levels of annular disruption and the pain score; using VAS of 6/10 or more at less or equal to 50 psi

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above opening pressure, they found that these parameters revealed negligible positive results at annular disruption below grade 3, and 44% positive results with grade 3 or greater annular disruption, with severe pain being proportional to the pressure in grade 4 and 5 discs.80 Subsequent to this study, Carragee and coworkers found the false-positive rate of low-pressure painful disc stimulation injections in subjects without chronic NSLBP to be about 25%.20 However, there were some drawbacks in this retrospective study including that some of these subjects had undergone previous back surgery. The conclusion from this study is that although the falsepositive rate of PD may be as high as 25% in an imperfectly selected asymptomatic population, this figure is likely to be less in subjects who do not have a chronic pain state or who have not had previous spinal surgery. In an effort to decrease the rate of false-positive findings, the methodology of discography is undergoing modification. The development currently is in AD, in which various local anesthetic agents are injected into the disc, and FAD, in which a balloon-tipped catheter is placed into the disc so that provocation maneuvers can be undertaken in the recovery room.81,82

Clinical Application By the time the specialist interventional clinician sees a patient with chronic severe recalcitrant NSSP, this patient will have usually seen numerous doctors, manual therapists and other health practitioners, had a variety of treatments, and be utterly confused about diagnosis and treatment. By this time, the patient often wants to understand the problem. Although different theories and models abound, an approach that is pathologically based and underpinned by anatomy has some logic and merit. Patients seem to understand this model when it is explained. At this stage of management, there are two divergent pathways. The first is to cease further attempts at diagnosis and treatment and to continue to manage the problem using pain management principles. The second is to attempt to make a tissue-specific diagnosis and as a result, to deliver a target-specific interventional treatment, despite the fact that the assessment leads to a good outcome in less than 50% of cases. The procession into this type of management should be understood by patient and clinician to be somewhat experimental. Patients should be alerted to the fact that the discography is a controversial test and that the management of IDD is contentious.79 Some basic issues that need to be understood by the patient at this stage include an understanding of referred pain and of the relative uselessness of special tests in the diagnosis of these referred pain problems.

Referred Pain is not the Same as Radicular Pain In presentations of axial pain, one major hurdle for the patient to overcome is the differentiation of referred pain from radicular pain. Most patients seem to consider that if the pain travels into the leg from the back that it is sciatica caused by a “pinched” nerve. It is important to understand the concept of referred pain because most pain in the limbs from the spine is referred pain. Radicular pain is relatively uncommon. One simple example of referred pain is angina, and this is a good model to discuss to indicate to the patient that limb pain can come from structures other than nerves.

Special Tests Rarely Substantiate a Diagnosis As discussed earlier, MRI, the most morphologically accurate test, can be used to identify profiles that render a patient more likely to have a positive discogram or at least an increased likelihood of NSLBP. MRI and other tests cannot provide a definitive diagnosis of pain pathophysiology or source in a patient with NSSP. Most patients have had or want MRI, and most have had plain x-rays and CT scans. Often they have been provided with an imaging-derived morphologic diagnosis, such as disc degeneration or facet joint degeneration, or the more pejorative and equally illegitimate label, “disc degenerative disease.” Perhaps even worse, they might have been labeled with the more personally challenging negative finding; “we have not found anything at all wrong on these tests,” which might have the implication that the pain is invented or at least “psychological.” These tests should be understood for what they achieve. First, they have a varied ability to exclude red-flag conditions. ­Second, they are particularly useful as a tool to establish the cause of radicular pain. Third, by and large they cannot establish the cause of NSSP.

Diagnosis is Rarely Tissue or Pathology Specific Diagnosis is particularly vexing; it needs to be accepted by all that in pain practice, diagnosis is often generalized to descriptions of the pain itself, and that illegitimate labels abound. NSSP is one label that can be used for a presentation of spinal somatic referred pain that is not caused by any other process or named condition. NSSP means pain, be it local or referred, that appears to derive from one of the locally innervated structures of the spine and does not derive from any known pathologic process. The prime indication for discography is NSSP of sufficient longevity, dimension, and character that the clinician and the patient consider that some further step needs to be taken to achieve significant pain relief. There is no consensus regarding acceptable parameters above which discography might be performed. It is generally stated that a patient should have exhausted all conservative meas­ ures including multidisciplinary management, pain management programs, and rehabilitation before being considered for intervention including discography, and that the likely medium- to longterm scenario is for persistent substantial disability and pain. The problem for the clinician is what to recommend to a patient with chronic disabling NSLBP. Discography is useful only from an interventional perspective if it rules in or rules out some form of treatment; options are confined to intradiscal procedures and spinal surgery. But these treatments have not been shown to be effective for the general population of patients with DP established on PD. Conversely, rehabilitation and pain management programs also have not had significant impact on the management of NSSP,83-86 although exercise programs combined with fear-avoidance application have proven merit in the prevention of chronicity,87-91 and pain management programs are often recommended as being more effective than traditional medical conservative treatment for chronic pain in general.92 In any case, the decision to move into interventional management for any patient typically occurs after such attempts have failed. Predicting long-term outcome is probably impossible in individual cases. Trends exist: but the course of back pain is not as optimistic as has been conveyed.93 Although about 76% of patients with a history of recent (within 6 months) low back pain recover or have low levels of pain, 14% have persistent, high disability with moderate-to-severe limitation of function.94

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Will the patient with severe disabling back pain ever get better? Many do not; however, some do. Smith performed a retrospective study of 25 NSLBP patients with positive PD in whom surgery was considered to be indicated yet was not undertaken.95 At a mean follow-up time of 5 years, 68% had improved, 8% were the same, and 24% had worsened. Of those who had become worse, 67% had psychiatric disease. As an aside, in this study 80% of those receiving workers’ compensation improved. If the patient does go to surgery consequent upon PD, what will be the long-term result? Knox and Chapman performed a retrospective study on 22 patients who had anterior lumbar interbody fusion for discogram-concordant lower back pain and found that all double level fusions did poorly and in single level fusions, 35% had good, 18% fair, and 47% poor results, with previous surgery and workers’ compensation doing the worst.96 Parker prospectively studied 23 patients treated by a single surgeon with posterolateral fusion.97 All underwent preoperative discography and were monitored for an average of 4 years postoperatively, at which time 39% had a good-to-excellent result, 13% a fair result, and 48% a poor result, with 90% of those on compensation having a poor result. Wetzel performed a retrospective review of 48 patients with low back pain who had discogram/CT, then lumbar arthrodesis, with a success rate (good outcome) of 46%.98 Carragee performed total discectomy and fusion on patients with positive discography and achieved highly effective outcome in 27% of patients, and minimally acceptable or better outcome in 43%.99 Is discography useful to detect pain possibly derived from discs adjacent to another disc that is to be fused? Willems found that PD adjacent to an intended to be fused segment (determined by temporary external transpedicular fixation) in patients with persistent back pain was not helpful and that patient outcomes after lumbar fusion were the same whether or not the adjacent disc was normal or degenerated.100 Discography has also been used as a pretest for intradiscal procedures including intradiscal electrothermal therapy (IDET) and nucleoplasty. Results from these procedures suggest that there may be cohorts within the IDD subtype that do well.101,102 What tests such as discography try to do is to develop a model that will predict which diagnostic subtype in which clinical scenario will do best with a particular treatment. It is a test that is not commonly performed; it is performed only on the most difficult presentations, and is done in interventional settings on a minimal number of patients presenting with spinal pain.

Can Other Tests Replace Discography? How Useful is MRI in the Assessment of NSSP and IDD? MRI changes occur in the asymptomatic population.51,103,104 In the lumbar spine, Boden and colleagues studied subjects with no past history of LBP and sciatica; in those younger than age 60, 20% had a herniated disc; in the 60 years and older group, 36% had a herniated disc and 21% had spinal stenosis. Disc degeneration or bulging at one or more levels occurred in 35% of subjects between 20 and 39 years, and in all but one of the subjects aged 60 to 80 years.103 MRI findings are common in asymptomatic individuals and the extent of changes is not predictive of the development or duration of future back pain.104 In the evolution of PD, attempts have been made to ascertain whether or not MRI can be used to predict PD outcome because PD

is not without morbidity.105,106 Although MRI is somewhat predictive of a positive PD test when a high intensity zone (HIZ) or Modic type I or II changes are found, it is somewhat insensitive. The HIZ, defined on sagittal MRI as a very bright signal (equal to or brighter than CSF on T2 weighted scans) contained within the posterior AF,17 has been shown to have appreciable but variable correlation with positive PD in patients presenting with NSLBP.79 The initial study showed that an HIZ increases the odds that PD will be positive in that patient at that level by a factor of 6.5.17 Studies on the HIZ since that time have all shown that HIZ is highly specific (range 0.74 to 0.93)107-111 but variable sensitivity, from as low as 0.09,108 to as high as 0.78.110 Thus, it is uncommon for an HIZ to occur in a disc that is not painful to PD, and the calculated likelihood ratios (ranging from 1.3 to 6.5 and averaging 4.1) indicate that an HIZ increases the odds that a PD will be positive by at least 50%.79 Additionally, although HIZs are present in both asympto­ matic and symptomatic subjects, they are found significantly more in symptomatic (prevalence 60% ± 15%) than asymptomatic subjects (24% ± 11%).112 Modic changes have also been studied in relationship to NSLBP and PD.113,114 The overall rate of vertebral end-plate signal changes (VEPSC) is about 43% in patients with NSLBP and 6% in those without.115 The most common association of VEPSC and NSLBP is extensive Modic type I changes at L5-S1.116 Overall, VEPSCs are relatively insensitive, but quite specific, for the diagnosis of IDD established by discography, with sensitivity of 23.2%, specificity 96.8%, PPV 91.3%, and NPV 46.5% in one study.25 When Modic changes are studied according to type, the type I end plate has the highest PPV for positive PD at 81% (±7%).114 It is possible for PD to be positive in the presence of a normal MRI. Zucherman reported on 18 symptomatic patients who had positive PD an average of 2.5 months after a normal MRI; positive meant production of concordant pain and abnormal disc morphology.117 This study was performed more than 20 years ago and whether or not this applies with current MRI technology is unknown.

Can Clinical Tests Predict IDD? The prevalence of IDD in a population of NSLBP patients thought to have sufficient pain and disability to undergo PD is about 35%.118,119 The prevalence of IDD in a group of patients with positive clinical indicators increases to 52% to 69%.118 The centralization phenomenon, or pain centralization, which is the retreat of referred pain toward the spinal midline during specified clinical examination, a history of persistent pain between acute episodes, a significant loss of extension and a subjective report of so-named “vulnerability in the neutral zone” individually and in combination increase the likelihood of an eventual diagnosis of IDD in a group of highly disabled and psychosocially distressed patients with otherwise diagnosed NSLBP.118,120 Additionally, if vibration applied over individual spinous processes is considered a positive test, then the odds of a positive PD increases significantly.121,122

Technical Performance of Discography Optimal lumbar discography is based on consensus guidelines published by International Spine Intervention Society (ISIS). However, optimal technique is uncommon; in a survey of physicians performing discography, the adherence to patient safety guidelines were as follows: preoperative antibiotics (83.81%), intradiscal antibiotics

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(84.97%), postprocedure antibiotics (9.82%), double-needle technique (64.16%). Additionally, the adherence to technical guidelines were as follows: optional use of CT scan (64.78%), pain assessment sheet (66.47%), entering on the side opposite symptoms (48.55%), manometry for opening pressure (65.31%), manometry of pain reproduction pressure (72.25%), injecting a control disc first (78.61%), injecting discs adjacent to the painful disc (56.64%).119 It is also evident that there is considerable variation from one specialty to another in discography performance.119

Interpretation of Discography There are three cardinal components that need to be recorded separately but viewed collectively; (1) provocation/analgesia, (2) disc manometry, and (3) disc morphology. These three different aspects are required to write a discogram report, and all three elements are still evolving. The International Spine Intervention Society (ISIS) describes positive PD as follows:49 (1) reproduction of the patient’s pain by stimulation of the affected disc; (2) such that the evoked pain has an intensity of at least 7 on a 10-point scale; and (3) pain is reproduced at a pressure of stimulation of <15 psi; (4) provided that stimulation of adjacent discs does not reproduce pain; and (5) postdiscography CT demonstrates a grade 3 or 4 fissure.

Provocation/Analgesia Assessment Although this phase occurs as the last step in discography, it is the most important aspect to record because it, above all, is the component that separates discography from other tests. Because this phase requires the patient to report subjective pain responses, it is open to reporting bias and other error. The optimal setting for the provocation component of discography is as follows: (1) the patient needs to be calm and comfortable, (2) the person recording the information from the patient should not be the injector, (3) that person and the patient should be blinded to the disc being injected. The degree of pain production should be recorded. It is not possible in many instances to use a visual analog scale in the operating room during the procedure. If so, a verbal pain rating is used. The patient should understand beforehand that this is to be used and it should be ascertained that the patient understands how to communicate pain with 0 to 10 as being no pain and 10 of 10 being the most severe pain that he or she can imagine. An example of the recording that can be used for PD is: P0 No pain response is noted on injection or distention of the disc. P± An equivocal response; vague, uncharacteristic, or discordant pain both by nature and location. P+ Definite, convincing pain provocation that is familiar to the patient yet only reproduces part of the symptom complex. P++ Exact pain reproduction, concordant with the symptom complex. Analgesic response can be recorded as follows (R if for response): R0 No change in pain after injection. R± A vague, uncertain response, denoted as less than 2 on a 10-point VAS scale. R+ A definite improvement of all or part of the presenting symptoms by 2/10 or more on the VAS. R++ Complete relief of all or part of the manifesting symptoms.

Disc Manometry Disc manometry is an estimate of the hydrodynamic competence of a disc. It is formally measured with manometric pressure ­systems.13,123,124 In IDD, NP pressure decreases irregularly, and AF stresses rise. The depressurization of the NP reflects the degradation of the nuclear matrix, which can no longer retain water efficiently, to sustain axial loading. This results in extra load having to be borne by the posterior AF. Both of these findings correlate with a positive provocation component.125

Disc Morphology The morphology of the disc is revealed during the contrast injection phase of discography. Under image intensification, AP and lateral views are used routinely. In a normal discogram, contrast remains contained within the NP, and it has smooth, regular margins. When abnormal, contrast is seen to flow from the NP into the AF, and when the disc is ruptured it flows into the epidural space. Postdiscography CT scan performed within 3 hours of the procedure provides more information about disc morphology and is said to improve diagnostic accuracy, at least for disc prolapse.126 CT-discography importantly provides a better ability to subtype PD according to the Dallas system.16 Where CT is not available, caudad gantry views can show the discs close to AP.

Cervical and Thoracic Discography It is not possible to determine if a cervical disc is a major source of pain using MRI or other imaging techniques, particularly as MRI findings do not correlate well even with advanced histologic DD.127,128 However, the cervical disc is likely to be a source of pain. If cervical DP is diagnosed, the ability of such knowledge to improve outcome in the management of neck pain is questionable.129-136 Cervical discography has hardly been studied,137 but has advocates. A review of cervical provocation discography, which includes disc stimulation and morphologic evaluation, found that there were few studies of good standard, and concluded the cervical discography is a useful tool for evaluating chronic cervical pain, without disc herniation or radiculitis, with the strength of evidence for diagnostic accuracy being at Level II-2.138 However, because the morphology of the cervical disc is substantially different from the lumbar disc, no comparative conclusions can be made from the studies on lumbar discography. The cervical AF does not consist of concentric laminae of collagen fibers as in lumbar discs; it is a crescentic mass of collagen that is thick anteriorly and tapers laterally toward the uncinate processes, and is deficient posterolaterally.114 There are no established postdiscography CT scan findings such as is seen in the Dallas description of these in the lumbar spine. There are no clinicopathologic correlations that underpin cervical, or thoracic, discography. The technique of cervical provocation discography was first published in 1957,139 having been pioneered by Cloward,140 and subsequently developed.141-144 In the lumbar spine, abnormal morphology and precise pain reproduction are two of the more important components that contribute to a positive discogram.145 This is not the case in the cervical spine because fissuring of cervical discs is not reflective of trauma but of normal anatomy and aging,146-149 and, hence, extravasation of contrast from the disc in cervical discography cannot be considered to be indicative of an abnormal disc.149-152 The essential component of cervical discography is, therefore, not morphologic, but it is in what happens

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during the injection or “stimulation” phase because stimulation of cervical discs in asymptomatic volunteers is painless or only minimally painful,148 meaning that cervical disc stimulation has at least some negative predictive value: if the disc does not hurt when stimulated, it is unlikely to be a source of pain. Additionally, to diminish the possibility of false positives, subsequent opinion and study has discerned that adjacent structures should be similarly stimulated to ensure that pain is not apparent in ­multiple sites. If cervical discography is used, it should be understood that it is in the very experimental stage of evolution. If performed, the recommended protocol is to perform multilevel procedures that stimulate pain: positive disc stimulation occurs when: (1) provocation of the target disc reproduces the patient’s (concordant) pain, and (2) adjacent site stimulation does not reproduce pain.153 It is evident from the use of cervical facet joint blocks and disc stimulation that more than one source of pain can be detected at any one cervical intervertebral segment.154 As a consequence, when disc stimulation is used, a positive test requires: (1) reproduction of the patient’s concordant pain at a magnitude of at least 7 on a 10-point VAS, (2) exclusion of cervical facet joint pain at any segmental level where disc stimulation is positive because the false-positive rate without exclusion is 67%,154 and (3) not finding reproduction of the patient’s pain in adjacent structures. Thoracic discography is even less studied. In a study on 10 asymptomatic subjects and 10 patients with chronic thoracic pain undergoing PD, it was found that: (1) even in asymptomatic people, thoracic discography could be intensely painful, especially when prominent Schmorl nodes were present, (2) MRI changes did not always correlate with disc morphology on discography, and (3) in the symptomatic group, 50% of studied discs were concordantly painful.155

Complications of Discography Discitis The use of sterile technique and single- or double-needle technique seem to be the minimum requirements for the prevention of infection. Prophylactic antibiotics may decrease the incidence of discitis. Discitis is a nasty complication. A review of cases revealed the following:156 It is accompanied by, at times, severe exacerbation of local pain. There is an accompanying but delayed rise in ESR—averaging 20 days to reach a peak. ll Bone scan changes peak at about 33 days, and at 18 days it is more common to have no bone scan changes. ll MRI changes are also delayed, and if they occur in the first 2 to 3 weeks postdiscography they are likely to represent new pathology.157 ll The course of lumbar discitis ranges from 8 to 11 weeks. ll The course of cervical discitis ranges from 6 to 7 weeks—usually resulting in spontaneous fusion. ll ll

There are no randomized or controlled trials on the efficacy of prophylactic antibiotics.158 Based on animal experiments,106 the incidence of postdiscography discitis is lowered with the use of cefazolin given intravenously or in the intradiscal suspension injection. In high concentrations, contrast medium can itself inhibit bacterial growth at least to some degree, and it does not reduce the inhibitory effect of antibiotics.159 A follow-up of 127 consecutive patients having lumbar discography with contrast

containing cefazolin 1 mg/mL revealed no cases of discitis.121 Willems and colleagues had no cases of discitis when they performed two-needle technique discography without preemptive antibiotics on 200 patients and followed them all for a minimum period of 3 months.160 The reported overall incidence of discitis without prophylactic antibiotics is in the region of 0.25% of all patients or 0.094% of all discograms.160 It is of course important to know where the injectate is going. Initial injection of antibiotic containing material should not be made if the needle tip site is unknown. For example, intrathecal administration of cefazolin can be fatal.161

Can Discography Cause Harm? Experimental animal studies have revealed that disc puncture can induce accelerated disc degeneration. Carragee followed two matched cohorts of 75 each without serious LBP “illness.”105 Each subject was assessed with MRI and one group underwent L3-4, L4-5, and L5-S1 discography examination in 1997. Between 7 and 10 years after enrollment, each subject underwent a further MRI: 50 discography subjects and 52 control subjects were reassessed. The results were summarized as follows: (1) in all graded or measured parameters, discs that had been exposed to puncture and injection had greater progression of degenerative findings compared to control (noninjected) discs: progression of disc degeneration, 54 discs (35%) in the discography group compared to 21 (14%) in the control group; 55 new disc herniations in the discography group compared to 22 in the control group (2) new disc herniations were disproportionately found on the side of the AF puncture, (3) the quantitative measures of disc height and disc signal also showed significantly greater loss of disc height and signal intensity in the discography disc compared to the control disc. Additionally, discography can produce long-term pain in subjects with abnormal psychological profiles. A 12-month follow up of subjects without LBP revealed that no subject with normal psychometric testing had persistent pain after discography, but pain of those with abnormal psychometric test results reported significant new low back pain.162 These facts mean that discography should not be undertaken unless there are strong indications that the results will substantially alter the management and that the management changes have a reasonable chance of producing a far better outcome than might be obtained otherwise. The second part of this chapter discusses the technical and radiographic aspects of discography. REFERENCES    1. Mixter WJ, Barr JS. Ruptures of the intervertebral disc with involvement of the spinal canal. N Engl J Med. 1934;211:210-215.    2. Wood KB, Blair JM, Aepple DM, et al. The natural history of asymptomatic thoracic disc herniations. Spine. 1997;22:525-529.    3. Inman VT, Saunders JB. Anatomicophysiological aspects of injuries to the intervertebral disc. J Bone Joint Surg AM. 1947;29:461-465.    4. Falconer MA, McGeorge M, Begg AC. Observations on the cause and mechanism of symptom-production in sciatica and low-back pain. J Neurol Neurosurg Psychiat. 1948;11:13-26.    5. Wiberg G. Back pain in relation to the nerve supply of the intervertebral disc. Acta Orthop Scand. 1949;19:211-221.    6. Hirsch C, Ingelmark BE, Miller M. The anatomical basis for low back pain. Studies on the presence of sensory nerve endings in ligamentous, capsular and intervertebral disc structures in the human lumbar spine. Acta Orthop Scand. 1963;33:1-17.    7. Feinberg SB. The place of diskography in radiology as based on 2,320 cases. Am J Roentgenol Radium Ther Nucl Med. 1964;92:1275-1281.

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418  Spine 158. Sharma SK, Jones JO, Zeballos PP, et al. The prevention of discitis during discography. Spine J. 2009;9:936-943. 159. Langer RD, Usmani A, van Gorkom KN, et al. In vitro assessment of the antibiotic efficacy of contrast media and antibiotics and their combinations at various dilutions. Br J Radiol. 2010;83:394-400. 160. Willems PC, Jacobs W, Duinkerke ES, De Kleuver M. Lumbar discography: Should we use prophylactic antibiotics? A study of 435 consecutive discograms and a systematic review of the literature. J Spinal Disord Tech. 2004;17:243-247.

161. Boswell MV, Wolfe JR. Intrathecal cefazolin-induced seizures following attempted discography. Pain Physician. 2004;7:103-106. 162. Carragee EJ, Chen Y, Tanner CM, et al. Can discography cause longterm back symptoms in previously asymptomatic subjects? Spine. 2000;25:1803-1808.

PART B INTERVERTEBRAL DISC ACCESS AND STIMULATION: LUMBAR, THORACIC, AND CERVICAL Milton H. Landers, DO, PhD The mechanics of medicine must not be mistaken for the very essence of medicine, which is an art and not alone a science… Will medicine retain its identity if reduced to engineering. Abraham J. Heschel1 Provocation discography is a highly technical procedure and can provide unique, clinically significant, and useful information regarding the origin of a patient’s pain complaint. However, as with all facets of medicine, we must proceed only if the planned procedure is dedicated to the best interest of the patient involved. Low back pain commonly seen with referral into the hip, buttock and thigh, is a common malady afflicting ~15% of the adult population in any given year, and 80% will suffer from this symptom during their lifetime. It is well known that disc pain accounts for 39% of chronic low back pain complaints,2 with zygapophysial3 and sacroiliac4 pain running a poor second and third. This makes pain from the lumbar disc the most commonly found and objectively determined source of low back pain. If a pain specialist is not trained to provide discography, or elects not to do so, this physician is unable to provide a diagnosis for approximately 40% of his patients suffering from this very prevalent complaint. The prevalence of discogenic thoracic pain is unknown, while the cervical spine, disc pain accounts for only16%, with zygapophysial pain approximately 65%.5 Although in the past it was argued that the intervertebral disc was devoid of innervation, presently, there is no doubt that the intervertebral discs are innervated6,7 and can therefore be the source of pain .Painful diseases of the disc associated with imaging pathology are well known, for example, discitis. However, it is also quite evident that asymptomatic patients are often are noted to have significant pathology on imaging studies. Pathology does not equal pain. MRI and CT imaging provide wonderfully detailed pictures of the spine, but they are merely images and provide only clues as to the pain generator. Stimulation of the intervertebral disc is the sole method of determining is the discs are painful under a mechanical load.

Indications Prior to the advent of modern imaging modalities, discography was proposed by Lindblum to diagnose protrusions and other changes in the outer disc morphology.8 With the current availability of CT

and MRI, discography is no longer indicated for diagnosis of radicular pain, sciatica, and elucidation of the external disc morphology. The indication for discography is to secure a diagnosis for somatic, chronic low back pain, with or without referral. It is used to determine which if any intervertebral discs produce pain with mechanical stimulation which is identical to the patient’s index pain complaint. The natural history of low back pain provides for significant improvement and often resolution within months; therefore discography is rarely indicated for pain of less than 3 months duration. The pain experienced should be of such a severity that it is interfering with activities of daily living and further intervention is required. In assessing a patient with low back pain, the results of a discogram must be interpreted and correlated in conjunction with the history, physical examination, psychiatric overlay, and other diagnostic modalities. Discography is frequently used to validate a surgical procedure. In that surgical success rates for low back pain, as determined by 5-year pain relief and functionality studies are not stellar, every patient with a positive discogram should not be considered a surgical candidate. Surgery for discogenic pain is a consequence of societal norms, unrealistic patient expectations and insistence, economic variables, medical legal concerns, medical referral patterns, and the proclivity of some surgeons towards highly invasive, extraordinarily well- reimbursed procedures.9 At the present time treatments for discogenic pain are limited, but new technologies including minimally invasive procedures and injectable therapies are being given a high priority and hopefully will see fruition in the coming years. However, lack of a validated, effective treatment does not negate the responsibility of the interventional pain physician to provide the patient with an accurate diagnosis. Discography must not be performed for capricious, unjustifiable reasons. For idiopathic low back pain, a well thought out algorithm must be utilized. The well respected International Spine Intervention Society (ISIS) has published such an algorithm based on the best evidence available.10 Discography should be considered the primary interventional diagnostic test when significant, chronic

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low back pain is present, the intervertebral discs are not pristine, and a diagnosis required. In addition, with regard to the societal cost of medical care, discography is a fiscally sound course of action in that a positive discogram essentially exits the patient from the interventional pain algorithm and prevents other questionable procedures, such as the ubiquitous, grossly over utilized interlaminar epidural steroid injection, from being foisted on a susceptible population.

Contraindications Absolute contraindications to the performance of discography at any level include (1) the patient being unable or unwilling to consent to the procedure; (2) inability to assess the patient response to the procedure, including sedation, significant analgesic use, or psychiatric overlay; (3) significant localized or systemic infection; and (4) pregnancy. Relative contraindications include (1) anticoagulant therapy or bleeding diathesis; (2) allergy to radiographic contrast, local anesthetic, or antibiotic; (3) anatomic derangements that would compromise the safe and successful conduct of the procedure. In regard to cervical discography, further contraindications exist. A case of iatrogenic quadriplegia has been reported2 owing to iatrogenic disc herniation and severe cord compression resulting from a disc injection at a level with little reserve space secondary to spinal stenosis. An anterior-posterior (AP) spinal canal diameter of less than 10 mm is an absolute contraindication, whereas an AP diameter of less than 11 mm constitutes a relative contraindication, to the performance of cervical discography at the specific or adjacent levels. To ascertain whether cervical discography is safe, the physician injectionist must personally interpret a recent MRI or CT scan to ensure that the cervical canal is ample.

Complications Prior to the routine use of prophylactic antibiotics, discitis was the most feared, although nonlife threatening, complication to disc access. However, with precautions as will be detailed subsequently, this problem has become exceedingly rare. A comprehensive discussion of complications attributable to discography, mild to severe, is beyond the scope of this chapter, and the reader is directed to several excellent reviews and papers on the subject.12-19

Equipment and Training Fluoroscopy equipment allowing for the requisite excellent imaging is a basic requirement for access to the intervertebral discs. The fluoroscopic instrument of choice is the C-arm, which can be moved in any plane to provide optimum imaging to direct needle insertion and to verify, and document, final needle position and contrast spread. C-arms, which can accommodate a 55-degree contralateral oblique provide greater and easier access and the ability to target either side. Radiation-saving modalities, such as low-dose, pulsed mode, collimation, and saving of last image are essential and ensure safe practice. Digital subtraction imaging (DSI) capability can often provide useful information, especially if the patient has undergone previous surgery with metallic hardware implanted. It is imperative that all physicians performing discography have training in the interpretation of real time fluoroscopic images whether cervical, thoracic, or lumbar. This training must be beyond the level of a residency and most current “pain” fellowships.

Expertise in radiologic interpretation is far beyond the training and proficiency of nurse anesthetists (CRNAs), physician assistants (PAs), and other so-called “mid level nonphysician providers.” To use the C-arm, an x-ray compatible procedure table is required. Although some operating room tables may suffice, most have metal incorporated into their structure which limits certain fluoroscopic projections. Carbon fiber tables, with the pedestal at the foot, are now quite affordable, and provide unlimited access and unrestricted imaging possibilities. Radiation safety precautions as discussed in Chapter 5 should be followed. In regard to radiographic guidance, although the use of computed tomography (CT), guidance has been advocated by a minority of practitioners,20 this technique should be avoided. Using CT allows one to accurately delineate the skin entry point, however the advancement of the needle toward the target is accomplished crudely, without imaging assistance. This adds to the physical discomfort of the patient, the time required to complete the procedure, and the chance for needle misadventures. CT necessitates the injection of contrast for verification of needle placement without the benefit of active, real time imaging. Therefore, during the injection phase of the procedure (i.e., disc stimulation) the emerging contrast pattern cannot be monitored for disruption of the annulus, endplate ruptures, and increase in height of the disc. In addition, vascular injections will, in all likelihood, escape detection owing to the rapid “washout” of contrast secondary to blood flow within the vein or artery. Marked increase in total radiation exposure to the patient is inherent in CT and should be of concern to all involved. There is no literary evidence indicating any benefit to the use of CT for discography. Specialty group guidelines published by the International Spine Intervention Society (ISIS)21 and the Physiatric Association of Spine, Sports, and Occupational Rehabilitation (PASSOR),22 ­specifically do not mention CT for use with disc access. A historical record of all procedures must be archived with hard or digital images. Multiple images must clearly identify that the needle is in safe position in AP and lateral projections prior to injection of contrast, and after disc stimulation by contrast injection.

Miscellaneous Supplies A variety of needles and syringes are required and vary as to the specific procedure level. This will be presented in the subsequent discussions. In addition to the specific procedure needles, a 25-gauge, 1.5-inch needle for skin localization and an 18-gauge needle for drawing up medications are used. A sterile, long, 8- to 12-inch, radio-opaque pointer, combined with a skin marking pen enables the injectionist to mark the proposed skin entry site in a sterile and radiation-safe manner. As of this date, only lumbar discography requires the use of manometry, although in rare cases, a 3 mL syringe may be considered appropriate but far short of the ideal. Many manometers both digital and analog can be purchased. Most are accurate to the degree required. Automated systems, which inject and record, are available but expensive and provide questionable benefit. For cervical and thoracic procedures, a 3 mL syringe fitted with short, lowvolume, small-bore extension tube is used: syringes smaller than 3 mL can exert too much pressure, whereas a 5 to 10 mL syringe is limited to the pressure that can be generated. Monitoring devices, such as pulse oximetry, noninvasive blood pressure, and ECG, must at the least be immediately available, and their use is required if any sedation is contemplated. An ongoing

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conversation with the patient is always an appropriate and accurate monitor of the patient’s comfort, level of consciousness, cardiac, and respiratory status pre-, peri-, and postprocedure. Whether the procedure is performed in an office, ambulatory surgery center, or hospital setting, emergency equipment, pharmaceuticals, oxygen, airway supplies, suction, and other resuscitation provisions must be immediately available and checked regularly to ensure proper functioning. In addition, trained personnel must be available in case of an emergency.

Intravenous Access Intravenous (IV) access is considered essential for discography. Although rare, emergent situations do occur and time restraints may not be ample to initiate IV access. Intravenous antibiotics (cefazolin 1 gram, gentamicin 80 mg, ciprofloxacin 400 mg) 15 to 30 minutes prior to needle insertion is standard of care. Although exceedingly rare, complications requiring the use of IV medications (allergic reactions, severe vasovagal reactions) do occur and IV access provides the possibility of nearly immediate treatment. In addition, discography is considered by many to be a highly stressful procedure and mild sedation is often provided.

Medications For patient comfort and acceptance, anesthetizing the skin and underlying tissues with lidocaine (Xylocaine) 1% prior to needle insertion is suggested. In cervical discography, for the majority of patients, the target structure lies within 1 inch of the skin surface. In this case, for needles larger than 25 gauge, a skin wheal alone will suffice. For lumbar and thoracic procedures however, when 18- or 22-gauge introducer needles are positioned close to the disc itself, a track of local anesthetic to the depth of the superior articular process provides excellent working conditions. This can be easily accomplished using a 25-gauge, 3.5 inch Quincke or Chiba spinal needle. In that the very name discography indicates an imaging study of the intervertebral disc, contrast is required to detail the internal disc architecture. Only nonionic, water-soluble contrast media should be used. Iohexol (Omnipaque) or iopamidol (Isovue) in concentrations of 180 to 240 mg/mL are safe with allergic reactions occurring in the 1:500,000 range. Contrast of the 300 mg/mL concentration, may be useful in cervical discography where the small volumes used may require a higher concentration for good visualization with fluoroscopy. Today, the addition of antibiotics to the contrast medium should be considered routine. The excellent paper by Klessig and colleagues23 details this practice. Gentamicin and cefazolin in a concentration of 1 mg/mL of contrast, or clindamycin 7.5 mg/mL exceeds the minimum inhibitory concentration of Staphylococcus aureus, Staphylococcus epidermidis, and Escherichia coli, the three most commonly implicated organisms in discitis events.

Sedation Although discography is an uncomfortable procedure, in competent hands, optimum sedation is often attained using minimal doses of pharmaceutical agents. Providing the patient with a detailed, honest account of the anticipated procedure during the consent phase of the interaction, “talking the patient through” the procedure (i.e., assuring that he/she is aware prior to any sensory stimulation,

engaging the patient in conversation, and perhaps using music, or other sensory stimulation as a mild distraction) is imperative to creating a compliant, relaxed patient. At all times during the course of the procedure, the patient must be able to converse with the attending physician. If not obtunded prior to any untoward event, the patient will often give a vocal warning of unintentional misplacement of the needle. However, when carried to a point where the patient is unresponsive or minimally responsive to painful stimuli, this degree of sedation must be considered as dangerous and is never appropriate. Intravenous midazolam is considered by many to be the perfect agent to provide a patient who is mildly sedated, but compliant. Excellent sedation is seen at doses in the range of 2.0 and 5.0 mg, often with a profound amnestic effect. Although not the choice of the author, some injectionists with an anesthesia background use the ultra–short-acting hypnotic, propofol. When given appropriately, the short half-life of this drug produces rapid, profound sedation for needle insertion, but rapid recovery for disc stimulation. It must be taken into consideration that high doses of any medication may lead to dysphoria, inability to respond to instructions, and noncompliant behavior. Unfortunately in many instances, sedation is used to conceal poor operator technique. Sedation can never take the place of technical competence. The use of opioids as a pre- and/or periprocedure medication for discography is a contentious subject. The essential endpoint of mechanical disc stimulation is the patient’s perception of significant concordant pain. By their very nature, opioids blunt the perception of pain. The provocation of pain during discography must be accurately assessed, compared and quantified by the  patient. The primary action of opioids will therefore lower the pain threshold, and the discomfort will be perceived as less severe. This may significantly alter the results of this diagnostic test. Therefore, use of even low-dose analgesic medications during discography will ensure a higher rate of false negatives. Conversely, some argue that providing a “small dose” of narcotics (fentanyl 50 mcg, meperidine 50 mg, or morphine 5 mg) prior to the procedure will help to decrease the rate of false positives in patients with clinically insignificant discogenic pain. For the sake of accuracy, possibly raising the standard for a positive discogram, from a VAS from 7/10 to 8/10, might be a more advantageous technique than through the use of unpredictable medications with wide variability in patient response. A diagnostic test is only as reliable as its accuracy, and opioids in any quantity degrade this quantitative data in an unpredictable manner. One often overlooked aspect concerning the use of significant sedation during discography is the expectation created by their use. During the consent phase prior to the procedure, the detailing of marked sedation provides validation of the patient’s expectation of a painful, brutal procedure, and creates the perception that the planned procedure is inherently excruciating to such a degree that significant sedation is required; this belief is self-fulfilling. In addition, the psychological overlay, often seen as a comorbid condition in the chronic pain patient, validates the patient’s idea of the extreme severity of the condition, in that a procedure that requires sedation must be unbearable. One problem facing discographers is that patients on chronic opioid therapy have developed some degree of altered pain response, including hyperalgesia and allodynia because of their long and often questionable narcotic treatment. Having these patients withdrawn entirely from their medications is often not an option. In this patient subset, provocation discography can be

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performed using their present state of medication load as a baseline pain level. Although quantification of their pain response might be difficult, determination of pain response to specific disc levels is often easily accomplished. When presenting these results to the referring physician or surgeon, the outcome must be understood in the context of the patient response to mild-to-moderate pain, such as creation of the local anesthetic skin wheal with a 25-gauge needle.

Preparation and Drapes Although the incidence of discitis is low, precautions must be taken, and a clean procedure or operating room is imperative. Aseptic technique must be adhered to using a sterile skin preparation with povidone-iodine, iodophor-alcohol (DuraPrep), or chlorhexidine and alcohol. Draping with sterile towels and fenestrated drapes provides a sterile field. Clean scrub suits for all those in attendance, and surgical caps and masks for those in proximity to the patient are prudent. Most discographers scrub, gown, and glove as for an open surgical procedure. A sterile cover for the C-arm image intensifier allows the physician to directly orient the image intensifier during the periprocedural period, and prevents contaminating detritus from falling onto the sterile field from the equipment.

Techniques Prior to beginning a discographic study, a decision as to what levels need to be included must be made. This selection is based on the physical examination, imaging studies, and patient sympto­ matology. Accurate pain referral maps are available for the cervical24-26 and thoracic27,28 regions and, although based on induced zygapophysial joint pain, appear to be accurate for intervertebral disc-mediated pain as well. In that negative control levels rostral and caudal to any substantiated painful disc provide an internal negative control validation, the suspected intervertebral disc and the two adjoining discs should be included. Although extraordinary exceptions may exist, disc stimulation of more than four levels is rarely indicated.

“core,” (i.e., internal disc disruptions), are prevalent in nearly all individuals older than 30 years of age. Pain can be elicited at nearly all levels. Therefore, the criteria for a positive level involve strict concordance of pain at a VAS of ≥7/10, and a negative internal anatomic control level. Multiple positive levels are frequently present.35

Lumbar Prior to the use of C-arms, biplanar fluoroscopy required the patient be positioned exactly to accommodate the radiographic equipment orientation. Today, the C-arm itself moves and can provide imaging in any plane. For lumbar discography, the patient is placed in prone position with a pillow or other apparatus placed under the lower abdomen to decrease the lordotic curve. Physiologic monitors are attached, and as described earlier, prophylactic antibiotic is given. Light sedation is initiated and the lower thoracic, lumbar, and sacral regions are “prepped and draped” as described previously. The lateral or extrapedicular approach to the lumbar intervertebral disc provides safe access with minimal morbidity (see Fig. 38-1). Historically, lumbar disc access was performed using a posterior, interpedicular, transdural approach. Because this technique requires puncture of the ventral and dorsal dura, it is used infrequently today except in those rare, very specific instances in which postsurgical changes or anatomic considerations necessitate. The lumbar spine is examined to ensure no segmental anomalies are present (see Fig. 38-2, A). Non–rib-bearing vertebral bodies are counted to ensure sacralized L5, or nonsacralized S1 vertebral bodies are identified. These important variants must be described on the procedure note. The targeted intervertebral discs are identified in AP view, and the C-arm is maneuvered in a cephalocaudal tilt motion so that the superior subchondral end plate of the vertebral body caudal

Criteria for Discogenic Pain The stricter the criteria for establishing a diagnosis, the fewer falsepositive results will occur. In the case of a diagnosis of discogenic pain, surgery of a highly invasive nature with the possibly of a lifelong disability may be based on the results; therefore strict criteria are mandated. For the lumbar spine: (1) the pain produced from the disc simulation must be concordant, exactly reproducing the patients ongoing index pain; (2) the pain on stimulation must be significant at a VAS of ≥7 on a scale of 10; (3) an internal anatomic control must be found where stimulation of an adjacent level is nonpainful or minimally painful29,30; (4) pain is noted at <50 psi above opening pressure; (5) except on rare occasions, pain occurs with a volume of contrast <3.5 mL; (6) internal disc disruption is noted preferably on a postprocedure CT scan, with a radial fissure to the outer third of the annulus (i.e., a grade 3 or higher lesion).31,32 Although there is little information regarding criteria for a positive thoracic discogram,33 using the preceding lumbar standards would be prudent at this time. The cervical intervertebral disc does not have a well defined nucleus which is bounded by an annulus.34 Fissures within the

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Figure 38-1  MRI axial T2W image through L4-5 intervertebral disc. Long arrow illustrates needle access into disc via the extrapedicular approach lateral to the superior articular process (SAP). Note annular tear, open arrow. IL, Iliocostalis lumborum; LL, Longissimus thoracis pars lumborum; M, ­Multifides; P, Psoas major.

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L4 L4 Figure 38-2  Anteroposterior (AP) scout image lumbar spine. A, Note that all end plates are seen as an oval (i.e., not parallel to x-ray beam). B, Note that the superior end plate of L4 is parallel to x-ray beam (arrow), while the inferior end plate of L4 appears as an oval.

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Figure 38-3  Right oblique image lumbar spine for L3-4 disc access. A, The superior end plate of L4 is parallel to x-ray beam (arrows). Superior articular process, SAP, of L4 appears under the midpoint of the L3 inferior end plate. Circle indicates target. Dashed black lines represent the L3 ventral ramus. B, A 25-gauge spinal needle is advanced down to the level of the SAP. Local anesthetic is injected during withdrawal to provide a track of insensate tissue. C, An 18-gauge introducer needle is advanced using “tunnel vision” lateral to the superior articular process (SAP). Dashed black line represents the L3 ventral ramus.

to the chosen disc is parallel to the x-ray beam. This end plate will be seen as a straight line rather than oval when in optimal position (see Fig. 38-2, B). The C-arm is then rotated in an oblique motion preferably contralateral to the side of the patient’s predominant pain complaint. This contralateral approach to disc puncture ensures that any pain reproduced during the stimulation phase of the procedure is actually due to the mechanical stress of the procedure and not the needle puncture itself. When the patient’s pain is central, bilaterally equal, or there are anatomic variations preventing access from one

side, needle insertion from either side is appropriate. In addition, many C-arm fluoroscopes will only provide a contralateral oblique view to 45 degrees, which is often not sufficient to provide satisfactory imaging at some levels and might require deviation from the “opposite side of pain” disc entry preference. After “squaring” the subchondral end plate, the C-arm is rotated until the superior articular process (SAP) of the level below appears to transect or lie under the midpoint of the inferior end plate of the level above (see Fig. 38-3, A). This imaging manipulation allows placement of the needle using “tunnel vision,” (i.e.,

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needle insertion parallel to the beam when the skin puncture site is aligned with the target endpoint). The needle will travel medial and caudal to the segmental ventral ramus, which courses medial to lateral, and dorsal to ventral through the foramen. Using this technique, the final needle tip position will be in the center of the nucleus when seen in an AP and lateral orientation. When the oblique view is perfected, the skin is marked overlying the target, just lateral to the SAP, and over the caudal aspect of the targeted disc. A skin wheal is made and a 25-gauge, 3.5 inch needle is advanced toward the lateral aspect of the SAP (see Fig. 38-3, B). The needle is then withdrawn slowly while injection of ~5 mL of lidocaine (Xylocaine) 1% provides an anesthetic track for further needle insertions. Care must be taken to ensure that local anesthetic is not placed within the intervertebral foramen. If foraminal spread of local anesthetic were to occur, the innervations of the intervertebral discs might be anesthetized, confounding the results obtained from the disc stimulation. Proponents of both single and dual needle lumbar discography techniques can be found. Prior to the use of prophylactic antibiotics, Fraser and colleagues36 reported an incidence of discitis of 2.7% using a single-needle technique with nonstylet needles versus 0.7% when an introducer needle was employed. However, using a single stylet needle technique, Professor Charles Aprill noted just one case of discitis in more than 2000 patients (<0.05% per patient). The author has accessed well over 5000 intervertebral discs without a single case of discitis (<0.02%) using a technique which will be described, calling for a skin puncture with a 15-gauge needle, 18-gauge introducer needle, 22-gauge disc puncture needle, and the use of both IV and intradiscal prophylactic antibiotics. The International Spine Intervention Society (ISIS)37 and the North American Spine Society (NASS)38 recommend the two-needle approach. In addition to the evidenced decrease in disc infection, the twoneedle technique offers several technical advantages. A single-needle technique involves the placement of 5 to 10 inch needles. Frequently, there is little space between the image intensifier and the patient. This is a benefit in that less scatter radiation is produced creating a safer environment; however, it can make manipulation of longer needles difficult. Whether due to the fluoroscopic equipment, patient body habitus, or working on the contralateral side from the C-arm, placing a shorter introducer needle first, prior to the disc puncture needle is an advantage. In that the dual needle technique enables the discographer to insert and position all introducer needles prior to engaging the intervertebral discs, and then advancing all disc puncture needles after changing to a lateral view, it is highly time efficient. Although the two-needle technique will be described subsequently, the single-needle approach is a viable alternative and is easily adapted because the same imaging views and basic technique are used. Single- or double-needle techniques at this juncture, must be considered a personal choice. Following localization of the skin and underlying structures, as noted earlier, a puncture is made with a 15- or 16-gauge, 1.5-inch needle. This prevents any needle that may come in contact with the disc from actually being passed through the skin. An introducer needle, 18 or 22 gauge and 3.5 or 5 inches long, is then advanced through the anesthetic track toward the lateral aspect of the SAP and toward the disc entry site (see Fig. 38-3, C). Advancement is halted when resistance is felt. This procedure is repeated until introducer needles have been placed at all levels to be tested see Figs. 38-4 and 38-5. A lateral view is then used to check needle depth (see Fig. 38-6).

The needle tips are usually seen near the posterior elements or within the dorsal and caudal intervertebral foramen. If the needle tips are at the posterior elements, they are advanced slowly into each foramen. Firm resistance will be felt if the disc is contacted and further advancement is stopped. If desired, an AP view will note all needles lying within each respective foramen at the lateral aspect of the intervertebral disc. Using active lateral fluoroscopy, the disc puncture needles, 22 or 25 gauge, 6 to 10 inches in length, are now individually inserted slowly through the introducer needle, and will be seen to traverse the foramen and felt to contact the intervertebral disc(see Figs. 38-7 to 38-9). To facilitate needle maneuverability and control, a slight bend on the disc puncture needle tip, opposite the bevel, is advocated. The L5-S1 intervertebral disc access is occasionally complicated by a “high” ilium preventing direct access to the center of the nucleus pulposus (see Fig. 38-10). This normal anatomic variant is much more common in men than in women. As illustrated in ­Figures 38-11 to 38-14, a curved needle technique can be used to provide adequate needle placement within the intervertebral disc. This variant requires the use of a dual-needle technique. In that the ventral ramus crosses the posterior aspect of each disc within the foramen, rarely during insertion of the needle is radicular-type dysesthesia noted by the patient. Further insertion of the needle should be stopped, and the needle withdrawn a slight amount. Because the ventral ramus lies lateral and cephalad to the course of the needle insertion, using the bend in the needle to proceed medially and caudally will often allow disc puncture without additional pain. If several attempts are made to bypass the nerve without success, the introducer needle can be withdrawn to the dorsal elements and redirected. In the majority of cases, detour around the ventral ramus can be accomplished by an experienced operator without significant difficulty. Because the outer third of the posterior annulus is innervated, some mild discomfort may be appreciated by the patient when the disc is contacted. This “pinch” will be axial in distribution often with radiation into the hip, buttock, and posterior thigh. It is easily distinguished from the lancinating, electrical type of pain noted if the ventral ramus is stimulated. Anecdotally, this twinge as the annulus is contacted appears to be common in those discs that later evidence pain on stimulation. Using active lateral fluoroscopy and the bent needle tip to maneuver within the substance of the disc, the needle is positioned into the center of each disc nucleus. AP and lateral images of needle placement are saved for documentation of acceptable needle placement prior to injection of contrast (see Fig. 38-15). When excellent needle position is noted within the disc nucleus, disc stimulation can commence. As indicated previously, injection is made using a manometer, with contrast containing antibiotic. The disc thought most likely to be positive from MRI pathology, should be stimulated last. The patient is blinded as to level and onset of stimulation. To ensure accurate visualization of the internal disc architecture during injection, the end plates of the contiguous vertebral bodies should be parallel to the beam. Injection into the disc is made slowly, in small aliquots of approximately 0.5 mL. Active fluoroscopy is used with many injectionists preferring a lateral view of the disc during active injection. The author prefers to use an AP view during injection in that it appears to provide a more accurate indication of the disc anatomy. Others suggest that a lateral view provides additional information about posterior annular disruptions. During injection, contrast should be noted within the nucleus (i.e., center of the disc) in AP and ­lateral views.

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Figure 38-4  Right oblique image lumbar spine for L4-5 disc access. A, The superior end plate of L5 is parallel to x-ray beam (arrows). Superior articular process (SAP), of L5 appears in optimal position under midpoint of the inferior end plate of L4. B, Note that the L3-4 needle was inserted at a different angle in three planes. Open circle indicates the introducer needle target. Dashed black lines represent the L4 ventral ramus. C, A 25-gauge spinal needle is advanced down to the level of the SAP. Local anesthetic is injected during withdrawal to provide a track of insensate tissue. D, An 18-gauge introducer needle is advanced using “tunnel vision” lateral to the SAP. Dashed black lines represent the L4 segmental nerve.

Injection proceeds until one of several endpoints is noted: significant pain ≥7/10 is produced; volume of injected contrast reaches 3.5 mL; significant extradiscal contrast is noted; or a pressure of ~90 pounds per square inch (psi) is attained. Repetition of the injection can be considered as required after a period of approximately 5 minutes. Occasionally, due to marked incompetence of the annulus, pressurization cannot be maintained. In these cases, a rapid bolus of contrast to provide a transient pressure increase might be entertained. Following disc stimulation, AP and lateral images are saved for the permanent medical record (see Figs. 38-16 to 38-19). During injection, operating room personnel record on a standardized form, the parameters as the injection proceeds. Important objective, quantitative data must be documented to validate the procedure. At a minimum, opening pressure, pressure at significant pain production, pain level, concordance of stimulated pain with the usual complaint, volume of injectate used, and description of contrast pattern must be recorded and added to the postprocedure

note as part of the historical record. In addition, subjective information such as vocal or physical pain responses, patient tolerance of local anesthetic infiltrate, and any other observations that might be useful for future consideration should be noted in procedure note. AP and lateral images of the postinjection discs are archived. In intervertebral discs shown to be positive, analgesic discography has been advocated by some.39,40 This entails injection of local anesthetic into the disc shown to provoke pain on stimulation. Significant decrease in pain is assumed to confirm the results of the provocation test. A recent multicenter study41 evaluating so called functional analgesic discography (FAD) using balloon tipped catheters inserted into the intervertebral discs shows only 39% of patients with positive provocation disc stimulation evidencing ≥75% relief with local anesthetic. Following the disc provocation phase of the procedure, the needles are removed, the back is cleaned of the dried preparation solution, sterile self-adhesive dressings are applied, and analgesia is provided as necessary.

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Figure 38-5  Right oblique image lumbar spine at L5-S1 level. A, Neither the superior end plate of S1 nor the inferior end plate of L5 is parallel to the beam. B, The superior end plate of S1 is ­parallel to the x-ray beam (arrows). Superior anterior process (SAP) of S1 appears lateral to the optimum position. C, Further obliquity is not possible secondary to a “high” ilium (arrows). The SAP of L5 appears lateral to the optimum position (black transecting line). Ventral ramus of L5 is represented by black dashed lines. D, A 25-gauge spinal needle (arrow) is advanced down to the level of the SAP. Local anesthetic is injected during withdrawal to provide a track of insensate tissue. E, An 18-gauge introducer needle is advanced using “tunnel vision” lateral to the SAP. Ventral ramus of L5 is represented by black dashed lines. The arrow points to the tip of the needle, which is positioned medial to the segmental nerve.

L4

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Figure 38-6  A, Anteroposterior (AP) image of the lumbar spine. All introducer needles are in place lateral to the intervertebral disc annulus. B, Lateral view with all introducer needles dorsal to the intervertebral disc annulus and within the caudal aspect of their respective foramina.

426  Spine

L3

L3

Figure 38-7  Lateral view of the L3-4 intervertebral disc. A, ­Introducer needle in place ventral to the posterior elements. B, Using active lateral fluoroscopy, the 22-gauge disc puncture needle was inserted through the introducer needle, penetrated the annulus, and was advanced into the center of the disc (i.e., the nucleus pulposus).

L4

L4

A

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L4

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L5

Figure 38-8  Lateral view of the L4-5 intervertebral disc. A, ­Introducer ­needle in place ventral to the dorsal elements and dorsal to the disc annulus. B, Using active lateral ­fluoroscopy, the 22-gauge disc puncture needle was inserted through the introducer needle, penetrated the annulus, and was advanced into the center of the disc (i.e., the nucleus pulposus).

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Figure 38-9  Lateral view of the L5-S1. A, Intervertebral disc with the introducer needle in place. B, Using active lateral fluoroscopy, the 22-gauge disc puncture needle was inserted through the introducer needle, penetrated the annulus, and was advanced into the center of the disc (i.e., the nucleus pulposus). Note that the needle entering the disc is slightly curved (arrow). Because the high ilium required the introducer needle to be inserted medial to the optimum skin entry point, the final tip position was lateral within the disc. A curved disc puncture needle was used to guide the needle into a midline position within the disc.  A significant curve on the disc puncture needle was used to position the needle within the middle of the nucleus pulposis.

Discography  427

Postprocedure Following the procedure, the patient is taken to recovery. Results of the procedure are discussed realizing that the medications used for sedation may render the patient amnestic. If positive concordant

L4

L5 I SAP S1

pain was noted at any level, a CT scan to document grade of annular disruption can be considered (see Fig. 38-19). Although at one point, CT postdiscography was the norm, with discography becoming routine, and being performed in offices and ambulatory surgery centers without CT capabilities, CT imaging can no longer be thought of as an absolute requirement. However, if significant concordant pain is noted during disc stimulation, but disruption of the annulus is not evident with fluoroscopy, a CT scan is mandated because occasionally, a very small tear is not evident on fluoroscopy but is apparent on axial CT views. When stable, the patient is discharged from the facility with postprocedure instructions. Driving should be curtailed for the day of the procedure. Some mild increase in the patient’s basal low back pain level is to be expected for a day or two. This increase is rarely severe and can be well managed with a prescription for a small amount of oral analgesics. The patient is provided with instructions for discussion of procedure results with the injectionist or the referring physician. As with all medical procedures, a true and accurate post procedure report must be generated by the discographer. This record must include all pertinent information and be of such detail that a reviewing physician can appreciate what actually occurred during the procedure itself. If a postprocedure CT was ordered, interpretation of this by the discographer is required. Correlation between the provocation discography and the CT images is essential and has validity only if performed by that physician involved with actually stimulating the intervertebral discs and evaluating the patient during the procedure. Interpretation by a noninvolved radiologist, separated by time and distance, is at best meaningless and inappropriate. See example in Appendix A.

Thoracic Discography Figure 38-10  Right oblique view of L5-S1 intervertebral disc with a “high” ilium (I) (white broken line). Further ipsilateral oblique movement of the fluoroscope will position the ilium further medial and overlie the target, just lateral to the SAP, preventing access to the disc. The tip of the SAP (short white line) is seen to lie in a lateral position in relation to the inferior end plate of L5 (long white line) rather than at the midpoint (short black line). By necessity, the skin entry site (small circle) is therefore medial to an optimum orientation and a needle driven without medial deviation will end up in the lateral aspect of the disc, probably in the annulus.

Literature pertaining to thoracic discography is limited to technical considerations.42,43 There is no evidence currently available on the validity and utility of this procedure. However, the thoracic intervertebral discs are in many ways analogous to the related lumbar structures; and negative stimulation is noted in seemingly nonpathologic discs and provocation of concordant pain in chronic thoracic pain patients can be frequently elicited—indications that

L4

L5 I SAP

S1 I

A

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Figure 38-11  A, Right oblique view of L5-S1 intervertebral disc with high ilium (I) (white ­broken line). ­Introducer needle is in ­position. B, Postprocedure CT with contrast noted within the nucleus pulposis. The black arrow represents a needle track that, as required, passes lateral to the SAP and is targeted toward the middle of the disc. Note that this proposed needle insertion would require it to pass through the ilium. A needle (white arrow) track passing lateral to the SAP and medial to the ilium would end up in the far lateral annulus. A curved needle technique will be required to access the nucleus pulposis.

38

428  Spine

L4

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Figure 38-12  Lateral views of L5-S1 disc with high ilium. A, Introducer needle in position. B, Disc puncture needle is advanced while introducer needle is withdrawn (black arrow), reinstitutes the curve (white arrow) placed on this needle prior to insertion. Curved trajectory will access the disc nucleus.

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thoracic discography appears to be an appropriate presumptive diagnostic procedure. Realization of the tentative nature of this procedure must be taken into account in regard to any clinical applications. The initial steps for thoracic discography are analogous to the lumbar procedure. Diagrams of referred pain patterns, MRI image review, and physical examination provide clues to the probable area to be investigated. The true incidence of thoracic discogenic pain is unknown. Because of the reluctance of surgeons to trespass into this area, discography is not frequently requested. However, in the future an increasing number of validated percutaneous procedures may increase the frequency of

Figure 38-13  Anteroposterior (AP) views of L5-S1 disc with high ilium.  A, Introducer needle (black arrow), and disc puncture needle with curve (white arrow) in position. B, Contrast, volume 0.5 mL in nucleus pulposus of L5-S1 disc. Significant positive concordant pain was noted.

this procedure. Nevertheless, a diagnosis for individuals with dorsal pain, with or without possible readily available treatment options, should not be dismissed as unimportant. Discography is purely a diagnostic procedure, and whether the outcome is positive or negative, a specific treatment modality is never mandated. As one progresses from lumbar, to thoracic, and finally to cervical interventional spine procedures, target structure size is reduced, tolerances become narrower, and the consequences of unintentional, errant needle placement become more profound. The injectionist contemplating thoracic procedures must assure himself of his expertise in interpreting the radiographic anatomy

Discography  429

38

(–) L4 Figure 38-14  A, Lateral view. Results of stimulation (±) noted. L5-S1 positive concordant pain at 0.5 and 0.75 mL. Pressure 2 ± 5 psi above opening. B, Postprocedure axial CT image, bone window of L5-S1 disc from Fig. 38-14, A. Access to the nucleus pulposis requires a curved disc puncture needle (depicted by the curved white line) be advanced through a larger bore introducer needle (straight white line). Broken black line represents a straight needle track coursing medial to the ilium and lateral to the SAP entering only the far right lateral aspect of the annulus.

(–) L5

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Figure 38-15  A and B, Final Anteroposterior (AP) and lateral views with all needles in excellent position within the nucleus pulposus at all disc levels.

Figure 38-16  A and B, Anteroposterior (AP) view of the L3-4 intervertebral disc pre- and postinjection of contrast. Note that the end plates of the L3-4 disc are parallel to the x-ray beam to afford an excellent view of the disc space.

430  Spine

A

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that will be encountered. Specifically, the dorsal region, the ribs, lungs, heart and other anatomic structures introduce a level of complexity which is unique to this area. Fluoroscopic images rarely provide the conspicuity as in the lumbar and cervical spine. The proximity of the pleura creates the real possibility of iatrogenic pneumothorax. Disc access in the thoracic spine involves needle introduction under conditions of close tolerances traversing a narrow corridor between rib head and superior articular process (see Fig. 38-20). Thoracic discography is technically demanding and should only be attempted by physicians whose skills have been well honed by extensive experience with fluoroscopically guided spinal procedures.

Equipment and Supplies Thoracic discography requires the same basic equipment and supplies as for lumbar, with a few changes. No literature exists as to the diagnostic benefit of using manometry in the thoracic spine. Unless the lower thoracic levels are a continuation of an upper lumbar study, manometry is merely an unproven option. However, it appears intuitive that a disc evidencing concordant pain at low pressure is of more significance than one requiring high pressure to

Figure 38-17  A and B, Anteroposterior (AP) view of the L4-5 intervertebral disc pre- and postinjection of contrast. Note that the end plates of the L4-5 disc are parallel to the x-ray beam to afford an excellent view of the disc space.

Figure 38-18  A and B, Anteroposterior (AP) view of the L5-S1 intervertebral disc pre- and postinjection of contrast. Note that the end plates of the L5-S1 disc are parallel to the x-ray beam to afford an excellent view of the disc space. Pathology is present at L5-S1 as compared to the L4-5 disc. Significant concordant pain was noted at 20 psi above an opening pressure of 7 psi.

elicit a response. Dual needle techniques are rarely used in the thoracic spine. Secondary to the anatomy, 3.5- or 5-inch needles can be used to access most thoracic intervertebral discs unless a patient of very large body habitus is being studied.

Procedure The patient is positioned prone on a radiolucent procedure table. Monitors are attached, IV antibiotic is provided, and mild sedation as above is initiated. Depending on the chosen procedure levels, the corresponding thoracic region is prepared and draped. In that most of the twelve thoracic levels are difficult to differentiate from each other, meticulous care must be taken to identify the targeted intervertebral discs. Counting down from T1, and then up from T12, should provided an identical answer. At each level to be studied, the end plates surrounding the disc are aligned so as to be parallel to the x-ray beam by using cephalocaudal tilt of the image intensifier (see Fig. 38-21). The end plates will evidence a linear rather than an oval appearance. As with the lumbar procedure, an oblique view is then used contralateral to the dominant pain (see Fig. 38-22, A). As the C-arm is rotated, the spinous process will appear to move toward the contralateral side, followed by the pedicle and

Discography  431

38

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A L3-4

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Figure 38-19  A through E, Anteroposterior (AP), lateral, and CT views postinjection. L3-4 and L4-5 evidence no sign of annular disruption. At L5-S1, a significant disruption of the normal internal disc architecture is noted in both AP, lateral, and CT image views (arrows). A broad grade 4 posterior annular disruption is noted.

S

R

Figure 38-20  CT image midthoracic spine postmyelogram. Possible disc access is noted on left between superior articular process (S) and rib (R).

rib head of the infrasegmental level. A hyperlucent rectangle, or “box,” will become distinct over the target disc. When the pedicle is seen to be positioned approximately 30% to 40% across the vertebral body further rotation should cease. The hyperlucent “magic box” will appear, and is easily identified over the disc with its sides defined rostrally by the inferior end plate of the vertebral body above; caudally by the superior end plate of the vertebral body below; laterally by the medial rib head line (i.e., a line oriented rostral-caudal connecting the medial aspect of the rib heads; and medially by the medial pedicular line which approximates the superior articular process and lamina which is at times quite indistinct (see Fig. 38-22, B). The skin is marked over the hyperlucent “box” and a local anesthetic skin wheal is made. A 25-gauge, 3.5-inch needle can now be advanced through the wheal toward the target and a local anesthetic track can be injected during withdrawal. A puncture can be made with an 18-gauge needle so that the disc puncture needle need not pierce and potentially carry skin and detritus into the disc. Depending on level and body habitus, a 22-gauge, 5-inch, or 25-gauge, 3.5-inch disc puncture needle, with slight bend at the tip opposite the bevel, is introduced and using the “tunnel vision,”

432  Spine

down the beam approach, guided toward the target “box” (see Fig. 38-22, C). The needle is incrementally advanced using intermittent fluoroscopy to make corrections. It is important to stay medial to the medial rib head line, the costovertebral joint, because the lung lies just lateral. Os is often contacted during needle advancement because the needle is transiting a space between rib head and superior articular process (see Fig. 38-20). If contact is made, withdrawing the needle tip from os 1 to 2 mm, rotating the needle and reinserting slowly, the bent needle tip will allow one passage

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Figure 38-21  Scout anteroposterior (AP) midthoracic spine. T6-7 disc end plates parallel to x-ray beam, arrows. Pedicle (P).

through this narrow space with minimal difficulty. Needle advancement is stopped when the intervertebral disc annulus is contacted as can be appreciated by its unique tactile feeling. The other levels are now accessed to the point of disc contact. When all needles are positioned in proximity to the discs (see Fig. 38-23), the C-arm is positioned for a lateral view, and the needles will be seen as aligned parallel to the respective vertebral end plates in the infraneural, caudal position within their foramen. The needles are then advanced slowly using active lateral fluoroscopy, using rotation to provide directional control secondary to the bent needle tips. The disc is felt and seen to be entered, and the needles are inserted sequentially into the center of the intervertebral discs. Needle position within the nucleus pulposus is then verified, and documentary AP and lateral images are saved (see Fig. 38-24). Injection of contrast with antibiotic is then made into each disc using active lateral imaging. The disc felt most likely to be positive by MRI pathology should be injected last. The patient is blinded as to level and onset of stimulation. As discussed previously, either a manometer is used, or 3 mL syringes with a smallbore, low-volume extension tubing. Tubing length must be limited in that perceived pressure increases in proportion to length. The injected volume into a thoracic disc will range from 0.5 to 2.5 mL depending on level, the more rostral discs resembling a cervical disc and accepting little volume. During injection, if a manometer is used, the same objective data as collected for lumbar discography is recorded. If one elects to use 3 mL syringes, approximate pressure generated, and characteristic of the endpoint (soft or firm) are recorded in lieu of opening and final pressure as determined with a manometer. AP and lateral images postcontrast are then saved (see Fig. 38-25, A and B). A true and exact, detailed procedure record of the entire procedure must be produced by the discographer as a historical documentation of the study. Postprocedure care is identical to that for lumbar discography. CT imaging postthoracic discography although never validated as having diagnostic utility, might be obtained if beneficial information is expected (see Fig. 38-25, C-E).

T7

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Figure 38-22  Right oblique. A, End plates of the T6-7 disc are parallel to the x-ray beam, arrows. Pedicle (P). Lateral pedicular and medial rib headlines are indicated by broken lines. B, Open arrow points to target “box”. Needle is in position at T7-8. C, Magnified right oblique thoracic spine. Needles are in position at T8-9 and T7-8.

Discography  433

Cervical spinal injections of any variety are “demanding, technically intensive, and unforgiving procedures”43 fraught with severe consequences at the slightest inadvertent misstep. Cervical discography should not be attempted by physicians of any primary specialty without extensive experience in fluoroscopically guided spine injection techniques and significant hands on instruction by an expert practitioner.

T6

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T8

As with all spinal injection techniques, cervical discography requires the use of a quality fluoroscope. Some physicians elect to place the fluoroscope at the head of the table rather than the side. This allows unrestricted positioning of the C-arm and excellent visualization of the cervical region in any plane. However, an x-ray compatible procedure table with the pedestal at the foot, allowing for unfettered, 360 degree access to the head of the bed must be available if this technique is used. Only the rare discographer elects to use manometry in the performance of cervical discography. Volumes are small, and the unique anatomy of the cervical intervertebral disc lends itself to manual pressurization. For each level to be injected, a 3 mL syringe with small-bore, low-volume extension tubing is used. Quincke tip spinal needles (25-gauge, 3.5 inches) are the ideal instrument for accessing the cervical intervertebral disc. Although in most cases the disc can be entered using a 2-inch needle, the longer needle provides the benefit of allowing ease of tubing attachment to the hub with less chance of needle displacement. Whereas iohexol or iopamidol contrast in the 200 to 240 concentration are acceptable, the 300 variety provides somewhat better visualization with the very small volumes used with this procedure.

Procedure

T9

T10

Figure 38-23  Right oblique thoracic spine. Needles are in position within the lateral annulus of intervertebral discs T6-7, T7-8, T8-9, and T9-10.

The patient is placed in supine position with a pillow under the shoulders to slightly extend the neck and the head is rotated slightly to the left. Monitors are attached, IV antibiotic is provided, and mild sedation as detailed earlier is initiated. After positioning, preprocedure fluoroscopic screening ensures adequate visualization of all planned levels in AP, lateral, and oblique views. Beards prevent adequate sterile preparation of the skin and must be removed before the procedure, preferably the day before. The cervical region is prepared and draped in a sterile manner. A wide preparation is advisable and should include the entire anterior and lateral neck, extend down to the clavicles, and

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38

Equipment and Supplies

Cervical

B

Figure 38-24  A, Lateral view thoracic spine. Needles have been advanced into the center of each disc. B, Anteroposterior (AP) view of thoracic spine. Needles are noted to lie in the center of each disc.

434  Spine

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Figure 38-25  A, Anteroposterior (AP) view of thoracic spine. Injection into (i.e., stimulation of) each disc has been completed. Concordant pain (+); No pain (−). B, Lateral view of thoracic spine. Injection into (i.e., stimulation of) each disc has been completed. Concordant pain (+); No pain (−). C, CT image T6-7. Disc stimulation (−). Note internal disc disruption (IDD) with negative stimulation. D, CT image T7-8. Disc stimulation (+) with IDD. E, CT image T8-9. Disc stimulation (+) with IDD. F, CT image T9-10. Disc stimulation (+) with IDD.

include the mandibular area. Both shoulders are incorporated so that the discographer can push the shoulders down manually if adequate visualization so demands. As with all spinal procedures, “An ounce of prevention is worth a pound of cure”. 45 Excellent discogenic pain referral maps for the cervical region are available,46 and will help guide the discographer; however, multilevel discogenic pain is common47 and a minimum of four levels should be studied to prevent omitting a painful disc and providing unreliable information. If pain is noted as referred into the occiput, C2-3 must be studied, whereas if scapular pain is present C6-7 is included. Unlike the thoracic and lumbar procedures, in cases of cervical pain, the zygapophysial joint must be evaluated prior to proceeding with provocation discography. An extraordinarily high falsepositive rate (68%) has been noted by Bogduk and Aprill,48 when cervical discography was not preceded by cervical medial branch anesthetic injections to block the segmental zygapophysial joints. In that the esophagus is prominent on the left, needle insertion is always from the right independent as to side of dominant pain.

The skin entry will be approximately along the medial border of the sternocleidomastoid muscle (see Fig. 38-26) but will vary slightly with the individual level. At the C6-7 level the apex of the lung, the thyroid, and common carotid arteries require a slight medial approach. The thyroid cartilage is present at C5-6 and will be readily evident if contacted on insertion, whereas a somewhat more lateral needle insertion is used at C2-3 to prevent entry and passage through a possibly distended hypopharynx. In the cervical region, due to the short distance between skin and intervertebral disc a dual needle technique is not advised. A slight bend on the 25-gauge procedure needle allows the operator to control direction during insertion. In addition, intradiscal manipulation is impossible without this needle modification. Any local anesthetic used must be limited to the skin because deeper infiltration may track along the cervical plexus or sympathetic chain and cause alteration in any pain response. With the patient positioned as above, the fluoroscope is obliqued toward the right into the so-called “foraminal view” where

Discography  435

38 Th SCM IJ

C

T E

Figure 38-26  Axial MRI T2 WI at C6-7 level with illustration of needle insertion. C, Carotid; E, Esophagus; IJ, Internal jugular; T, Trachea; Th, Thyroid; SCM, Sternocleidomastoid muscle.

the foramen are seen at their widest extent in both the cephalocaudal and ventral-dorsal dimensions. This is the same view advocated for cervical transforaminal and cervicothoracic (stellate) ganglion injections. The objective disc is identified by counting down from the readily identifiable C2-3 level, and the C-arm is manipulated so that end plates of the contiguous vertebral bodies are seen to be parallel to the x-ray beam. It must be emphasized that the course of the vertebral artery runs in a cephalocaudal orientation over the uncinate line (see Fig. 38-27). A target point is selected over the disc approximately one third the distance between the uncinate process and the apparent ventral disc margin (see Fig. 38-28, B). The skin entry site is marked, and will be seen to be medial to the sternocleidomastoid and carotid artery, which can be easily palpated. If desired, a small skin wheal is made with local anesthetic. Using a blunt sterile instrument, pressure is then applied over the insertion site to decrease the distance between the skin and disc and also to distract vulnerable soft tissue structures away from the needle track. The patient is asked to refrain from vocalization, swallowing, or coughing, and the needle is then quickly advanced over the tip of the blunt instrument, and using active fluoroscopy is maneuvered toward the disc in one fluid movement (see Fig. 38-28, C). Resistance to further insertion is noted as the needle enters the disc, and needle advancement is halted when purchase in the disc is accomplished. Total time elapsed between needle skin puncture and disc entry is often less than 2 seconds. During needle insertion, the bend on the needle tip allows precise directional control by rotation. Some radiation of the dominant hand is inevitable; however, using pulsed 8/second, and low-dose fluoroscopic modes, it is minimal and an acceptable risk. When needles are positioned in the periphery of all levels to be studied (see Fig. 38-28, D) the fluoroscope is rotated into a lateral view. Using active lateral fluoroscopy the needles are advanced into the approximate center of each disc and the position is verified in AP view. Care must be taken to ensure that the needle is not advanced through the disc, which could involve entry into the spinal canal and probable cord penetration. AP and lateral views

C3

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Figure 38-27  Scout image cervical spine “foraminal” view. Note inferior end plate of C5 and superior end plate of C6 are parallel to x-ray beam. Light dashed lines represent the position of the vertebral artery.

are then saved to document-safe needle position (see Fig. 38-29). At C6-7, if body habitus prevents adequate lateral visualization, AP, ipsilateral oblique, and contralateral oblique images can be substituted on the rare occasion. After the needle stylets are removed, the 3 mL syringes filled with contrast solution are connected to the hubs using the small-bore, minimal volume extension tubing, with Luer-Lok connections. Care must be taken to ensure that the needles are not advanced during the connection process. Active lateral fluoroscopy is the used during disc stimulation (i.e., injection of contrast). The patient is blinded as to level and onset of stimulation. Pressure of injection is slowly increased until the intrinsic internal pressure within the disc is overcome and a small amount of contrast is seen within the disc. At this point, injection is halted. Occasionally, some momentary pain will be felt by the patient at opening pressure. This is usually transient and is probably a response to enlargement of a fissure. If high pressure is evident without intradiscal contrast noted, the needle opening may be lodged in dense discal material. Slight withdrawal of the needle and repositioning within the disc will often rectify this problem. Prior to reinjection, safe needle position must be verified. When opening pressure has been noted, slow injection of contrast can proceed. Often firm resistance or pain will be noted with injection of as little as 0.2 mL. Injection into any nonpathologic cervical intervertebral disc will be limited to less than 0.5 mL and high pressure noted.49 Cervical intervertebral discs that appear to hold more than 0.5 mL will invariably be noted to have pathology on imaging. In normal discs, the endplates will be seen to separate owing to an increase in disc height during injection. AP and lateral images for the permanent medical record must be archived (see Fig. 38-31). During disc stimulation, the parameters of the injection are recorded on a standardized form by operating room personnel. At a minimum, volume of injectate, endpoint pressure (soft or firm), pain response (vocal or physical), pain intensity, and pain concordance are assessed. Endpoints of stimulation as per the ISIS guidelines cited previously include: concordant pain reproduced at a VAS of ≥7;

436  Spine

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C5 Figure 38-28  Cervical spine “foraminal” view. Needles have been previously placed in the C4-5 and C5-6 intervertebral discs. A, Image for C3-4 intervertebral disc access. Note inferior end plate of C3 and superior end plate of C4 are square to beam. B, Skin entry site is marked by pointer (i.e., blunt instrument). Target is in center of image to prevent insertion error due to parallax. C, To reduce the insertional distance, pressure is applied with the blunt instrument while the needle is quickly advanced into the C3-4 disc using active fluoroscopy. This allows for continuous directional control by rotation of the bent needle and prevents needle misadventure into potentially dangerous structures. D, Needle placed in lateral aspect of C3-4 intervertebral disc.

D

C2 C2

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Figure 38-29  A, Anteroposterior (AP) view of the ­cervical spine with needles in the ­center of the intervertebral discs prior to injection of contrast. B, Lateral view of the cervical spine with ­needles in the center of the intervertebral discs prior to injection of contrast.

B

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C6 Figure 38-30  A, C2-3 injection of contrast (i.e., disc stimulation). Note this is not a true lateral view in that the zygapophysial/facet joints and the neural arches show nonalignment of bone margins (arrows). B, True lateral image of C3-4 with injection of contrast (i.e., disc stimulation).

Discography  437

38 C2

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significant nonconcordant pain; neurologic symptoms experienced by the patient; contrast escaping from the disc; displacement of the vertebral body end plates; or firm resistance to injection. A positive level for discogenic pain is noted if concordant pain is evidenced with at least one asymptomatic, negative control level. Almost all cervical discs when stimulated to a sufficient level can produce pain whether pathologic or not. Evaluation of the procedure in regard to the patient’s response often requires experience beyond the technical considerations. Patients vary greatly in pain tolerance and psychological overlay, necessitating in the study results a certain degree of subjectivity by the discographer. Analgesic discography although first described in the cervical region as referenced earlier,26 has not been validated as providing accurate information on which to base clinical decisions. Bogduk and Aprill34 were able to provide analgesia in only 7 of 34 (21%) of discs evidencing pain on stimulation, which only comes close to the level of placebo effect. Further study is needed. Various patterns of contrast spread are expected even in asymptomatic cervical discs. In that the majority of mature cervical intervertebral discs evidence fissures and other pathology of the internal disc architecture, this is of little consequence and does not enter into the evaluation. For this reason, in the majority of cases, postcervical discography CT scans are not indicated. Following the procedure an all-inclusive, highly detailed, individualized record of the procedure must be produced and archived. Post procedure care requires a prudent recovery period, and general instructions as noted for the lumbar procedure.

C6

Figure 38-31  A, Lateral image of cervical spine following disc ­stimulation. At C5-6, note marked spread in the uncovertebral fissure (i.e., joint of Luschka), evidence of disc maturation (arrows). B, Anteroposterior (AP) image of cervical spine following disc ­stimulation. At C5-6, note marked spread in the uncovertebral fissure (i.e., joint of Luschka), arrows.

Summary Provocation discography, whether cervical, thoracic, or lumbar, is a powerful diagnostic tool in the hands of the well-trained interventional pain physician. For the complaint of somatic low back pain, discography is the only diagnostic modality able to correlate the history, symptoms, and signs with direct mechanical stimulation of a suspected pain generator. It is a proactive study analogous to palpation and rightly belongs as a component of the physical examination. In that 40% of low back pain patients suffer from discogenic pain, it must be within the armamentarium of all who practice the specialty of interventional pain or nonsurgical spine management. As with any diagnostic test, false positive results will occur; however, if vigilance in regard to patient selection and meticulous procedural detail are adhered to, careful interpretation of the raw data, and adherence to published guidelines is maintained, this small false positive rate has been shown to be in a low but acceptable range. More than once since its inception, discography has been subjected to unfounded, often biased, attacks and declared dead. Similar to the zombie of lore, arising from its grave, each new generation resurrects this procedure and discovers it to be alive and valid. No doubt procedural nuances will be instituted in the future to further refine our use and interpretation of disc stimulation, and discography will continue to provide a diagnosis for and guidance in the treatment of our patients.

Example of Procedure Note for Lumbar Discography Patient: Mr. John Q. Pain Injectionist: Dr. Needle History: See previously dictated consultation. Mr. Pain suffers from low back pain, left greater than right, radiating into the hip, buttock, and posterior thigh for ~8 months. The pain is maintained at a 7 to 9/10 VAS and interferes with activities of daily living. Pain increases with sitting or walking, decreases temporarily with change of position or activity. There is no position of comfort. MRI evidences degenerative disc disease at L5-S1 and L4-5. A small midline protrusion without neural involvement and a high intensity zone is noted at L4-5. Preoperative diagnosis: ll ll

Low back pain with referral, etiology unknown Degenerative disc disease with HIZ Postoperative diagnosis:

Discogenic pain L4-5, low pressure with internal disc disruption ll Internal disc disruption without significant pain on disc stimulation L5-S1 ll

Procedures: Injection into lumbar intervertebral discs times three levels Lumbar discography, supervision and interpretation times three levels ll Sedation for 45 minutes ll ll

Procedure: Informed consent was obtained from the patient in regard to risks, complications, and alternatives. Discitis and the provocative nature of the study were discussed at length. Mr. Pain elected to proceed. He was taken to an operating room with IV in place. He was placed in prone position with a pillow under the abdomen to decrease the lordotic curve. Physiologic monitors were attached. Prophylactic cefazolin was given. Sedation with midazolam only was afforded. The patient was conversing throughout the procedure. The lower thoracic, lumbar, and sacral regions were prepped and draped in a sterile manner. A C-arm was used to examine the lumbar spine. Five lumbar, non–rib-bearing vertebral bodies were noted. The intervertebral discs at L3-4, L4-5, and L5-S1 were identified sequentially. At each level, the superior end plate of the level below the targeted disc was aligned parallel to the beam. A right oblique view was then obtained so that the superior articular process of the level below appeared to lie as closely as possible under the approximate midpoint of the inferior end plate of the level above. At each level sequentially, a skin wheal was made 438

A

with local anesthetic and carried down to the level of the superior articular process. A puncture was made with a 15-gauge needle, through which an 18-gauge introducer needle was passed using “tunnel vision” toward the lateral aspect of the superior articular process at each level. When all three introducer needles were in place, a lateral view evidenced all introducer needles as lying just ventral to the posterior elements. Using active lateral fluoroscopy, the 22-gauge disc puncture needles were advanced through the introducer needles and seen and felt to enter the intervertebral discs. The needles were advanced into the center of each disc. No dysesthetic radicular type pain was noted during insertion of any needle. An AP view indicated excellent needle position at all levels. Injection was then made into each disc using an injectate of iopamidol 200 containing gentamicin 2 mg/mL. A manometer was used. During injection, volume injected, opening pressure, final pressure, pain response, and contrast pattern were recorded. L3-4: Volume - 1.75 mL Opening pressure – 18 psi ll Final pressure – 90 psi ll Pain - none ll ll

Remarks - Contrast is noted within the nucleus pulposus in AP and lateral views. No annular disruption is present. L4-5: Volume - 1.25 mL Opening pressure – 12 psi ll Final pressure – 27 psi ll Pain - Concordant, 9/10 (VAS) with vocal and physical pain response. ll ll

Remarks - Contrast is noted within the nucleus pulposus. In lateral views, a posterior annular tear is noted. L5-S1: Volume - 2.75 mL Opening pressure – 8 psi ll Final pressure – 90 psi ll Pain - Nonconcordant, dissimilar pain, to right, 4/10 (VAS) ll Remarks - Contrast is noted within the nucleus pulposus. A degenerative pattern is noted. ll ll

Mr. Pain tolerated the procedure well, was taken to recovery, and then for a post-procedure CT scan. He will follow up with his primary care physician in the near future. A consultation with Dr. Surgeon might be considered to discuss possible surgical treatment options. Mr. Pain knows to follow up with this physician if any problems were to develop.

Discography  439

Interpretations of CT Post-Discography This interpretation should be considered the “Functional Report for the Record” and take precedence over all other previous and future interpretations because correlation with the provocative discography is an essential part of the interpretation and can only be afforded by the physician who actually injected the intervertebral discs. Scout sagital and 3 mm axial views through the lumbar cistern were examined on this date. Axial images included both bone and soft tissue windows and included contiguous slices, parallel to the end plates, through the intervertebral discs at L3-4, L4-5, and L5S1. Contrast was noted within the disc spaces of all levels listed above. L3-4: Contrast is noted within the nucleus pulposis. No annular disruption is present. This is a Grade 0 nuclear pattern. L4-5: Contrast is noted within the nucleus pulposos. A Grade 4 radial posterior annular tear toward the left is evident with an associated small protrusion. L5-S1: Contrast is noted within the intervertebral disc space. No discrete annular tear is evident; however, a Grade 3 degenerative pattern left greater than right is noted. Interpretation of Procedure 1. L3-4: No disruption of the normal internal disc architecture is evident on plain fluoroscopy or X ray. This is negative. 2. L4-5: Pressure of 12 psi. Significant disruption of the normal internal disc architecture is noted on both fluoroscopic and CT imaging. This is a positive level as per ISIS Guidelines. False positive reat 3% per Wolfer et al. 3. L5-S1: This is a negative level...disc architecture.

Mr. Pain and his wife were seen in recovery, and the results of the discogram were discussed. He will follow up with his primary care physician in the near future. A consultation with Dr. Surgeon might be considered to discuss possible surgical treatment options. Mr. Pain knows to follow up with his physician if any problems were to develop. Interpretation: L3-4. This is a negative level for discogenic pain. No pain was noted with disc stimulation up to 90 psi. No disruption of the normal internal disc architecture is evident. This is a negative level for discogenic pain without internal disc disruption, and provides a negative control level. L4-5. This is a positive level for discogenic pain. Marked concordant pain was noted at 15 psi above an opening pressure of 12  psi. This is a positive level for discogenic pain at low pressure stimulation, with internal disc disruption. It meets the highest criteria for discogenic pain as per ISIS guidelines. L5-S1. This is a negative level for discogenic pain. Although some discomfort was noted at 90 psi (i.e., 82 psi above an opening pressure of 8 psi, this pain was nonconcordant, at high pressure, and only at an intensity of 4/10 (VAS). This is a negative level for discogenic pain, with disruption of the normal internal disc architecture. Mr. Pain tolerated the procedure well, was taken to recovery, and then for a postprocedure CT scan. He will follow-up with his primary care physician in the near future. A consult with Dr. ­Surgeon might be considered to discuss possible surgical treatment options. Mr. Pain knows to follow-up with this physician if any problems were to develop.

REFERENCES   1. Heschel AJ. The Patient as a Person. San Francisco. American Medical Association Annual Meeting 1964. In: The Insecurity of Freedom: Essays on Existence. New York: Schochen; 1966:24-38.   2. Schwarzer AC, Aprill CN, Derby R, et al. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine. 1995;20:1878-1882.   3. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophysial joints. Is the lumbar facet syndrome a clinical entity. Spine. 1994;19:1132-1137.   4. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine. 1995;20:31-37.   5. Yin W, Bogduk N. The nature of neck pain in a private pain clinic in the United States. Spine. 2006;9:196-203.   6. Bogduk N, Tynan W, Wilson AS. The nerve supply to the lumbar intervertebral disc. J Anat. 1981;132:39-56.   7. Bogduk N. The innervations of the lumbar spine. Spine. 1983;8:286-293.   8. Lindblom K. Diagnostic puncture of the intervertebral discs in sciatica. Acta Orthop Scand. 1948;17:231.   9. Deyo RA, Mirza SK, Martin BI, et al. Trends, major medical complications, and charges associated with surgery for lumbar spinal stenosis in older adults. JAMA. 2010;303:1259-1265. 10. Algorthim for Investigation of Low Back Pain. In: Bogduk N, ed. Practice Guidelines for Spinal Diagnostic and Treatment Procedures. San Francisco: International Spine Intervention Society; 2005:87-94. 11. Laun A, Lorenz R, Agnoli AL. Complications of cervical discography. J Neurosurg Sci. 1981;25:17-20. 12. Aprill CA. Diagnostic Disc Injection. I. Cervical Disc Injection. In: Frymoyer JW, ed. The Adult Spine: Principles and Practice. Philadelphia: Lippincott-Raven; 1997:523-538. 13. Aprill CA. Diagnostic Disc Injection. II. Lumbar Disc Injection. In: Frymoyer JW, ed. The Adult Spine: Principles and Practice. Philadelphia: Lippincott-Raven; 1997:539-562. 14. Landers MH. Diskography. In: Waldman SW, ed. Pain Management. Philadelphia: Saunders-Elsevier; 2007:118-144.

15. Fraser RD, Osti OL, Vernon-Roberts B. Iatrogenic discitis: The role of intravenous antibiotics in prevention and treatment. An experimental study. Spine. 1989;14:1025. 16. Osti O, Fraser RD, Vernon-Roberts B. Discitis after discography. The role of prophylactic antibiotics. J Bone Joint Surg Br. 1990;72:271. 17. Connor PM, Darden BV 2nd. Cervical discography complications and clinical efficacy. Spine. 1993;18:2035. 18. Zeidman SM, Thompson K, Ducker TB. Complications of cervical discography: Analysis of 4400 diagnostic disc injections. Neurosurgery. 1995;37:414. 19. Boswell MV, Wolfe JR. Intrathecal cefazolin-induced seizures following attempted discography. Pain Physician. 2004;7:103. 20. Fenton DS, Czervionke LF. Discography. In: Fenton DS, Czervionke LF, eds. Image-Guided Spine Intervention. Philadelphia: Saunders; 2003:227-255. 21. Bogduk N, ed. Practice Guidelines: Spinal diagnostic & treatment procedures. San Francisco: International Spine Intervention Society; 2004. 22. Pauza KJ. PASSOR Educational Guidelines for the performance of spinal injection procedures. : PASSOR Board of Governors and AAPMR Board of Governors; 2001. 23. Klessig HT, Showsh SA, Sekorski A. The use of intradiscal antibiotics for discography: An in vitro study of gentamycin, cefazolin, and clindamycin. Spine. 2003;28:1735-1738. 24. Bogduk N, Marsland A. The cervical zygapophysial joints as a source of neck pain. Spine. 1988;13:610-617. 25. Dwyer A, Aprill C, Bogduk N. Cervical zygapophysial joint pain patterns. 1: A study in normal volunteers. Spine. 1990;15:453-457. 26. Fukui S, Ohseto K, Shiotani M, et al. Referred pain distribution of the cervical zygapophysial joints and cervical dorsal rami. Pain. 1996;68:79-83. 27. Fukui S, Ohseto K, Shiotani M. Patterns of pain induced by distending the thoracic zygapophysial joints. Reg Anesth. 1997;22:332-336. 28. Dreyfuss P, Tibiletti C, Dreyer SJ. Thoracic zygapophysial joint pain patterns. A study in normal volunteers. Spine. 1994;19:807-811.

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440  Spine 29. Lumbar disc stimulation (Provocation Discography). In: Bogduk N, ed. Practice Guidelines: Spinal diagnostic & treatment procedures. San Francisco: International Spine Intervention Society; 2004:20-46. 30. Mersky H, Bogduk N, eds. Classification of Chronic Pain. Descriptions of chronic pain syndromes and definition of pain terms. 2nd ed. Seattle: IASP Press; 1994:180-181. 31. Moneta GB, Videman T, Kaivanto K, et al. Reported pain during lumbar discography as a function of annular ruptures and disc degeneration. A re-analysis of 833 discograms. Spine. 1994;17:1968-1974. 32. Sachs BL, Vanharanta H, Spivey MA, et al. Dallas discogram description: A new classification of CT/discography in low back disorders. Spine. 1987;12:287-294. 33. Bogduk N, ed. Thoracic provocation discography Practice Guidelines: In Spinal diagnostic & treatment procedures. San Francisco: International Spine Intervention Society; 2004:287-313. 34. Mercer S, Bogduk N. The ligaments and annulus fibrosus of human adult cervical intervertebral discs. Spine. 1999;24:619. 35. Cervical disc stimulation (provocation discography). In: Bogduk N, ed. Practice Guidelines: In Spinal diagnostic & treatment procedures. San Francisco: International Spine Intervention Society; 2004:95-111. 36. Fraser RD, Osti OL, Vernon-Roberts B. Discitis after discography. J Bone Joint Surg Br. 1987;69:26-35. 37. Lumbar disc stimulation (Provocation Discography). In: Bogduk N, ed. Practice Guidelines: Spinal diagnostic & treatment procedures. San Francisco: International Spine Intervention Society; 2004:20-46. 38. Guyer RD, Ohnmeiss DD. Lumbar discography: position statement from the North American Spine Society Diagnostic and Therapeutic Committee. Spine. 1995;20:2048-2059.

39. Roth DA. Cervical analgesic discography. A new test for the definitive diagnosis of painful-disk syndrome. JAMA. 1976;235:1713. 40. Ohtori S, Kinoshita T, Nakamura S, et al. Surgical results for discogenic low back pain randomized study using discography vs. discoblock. Spineweek 5/29/2008. 2008:59. 41. DePalma MJ, Lee JE, Peterson L, et al. Are outer annular fissures stimulated during diskcography the source of diskogenic low-back pain? An analysis of analgesic diskography data. Pain Medicine. 2009;10:488-494. 42. Schellhas KP, Pollei SR, Dorwart RH. Thoracic discography: A safe and reliable technique. Spine. 1994;19:2103-2109. 43. Thoracic provocation discography Practice Guidelines. In: Bogduk N, ed. Spinal diagnostic & treatment procedures. San Francisco: International Spine Intervention Society; 2004:287-313. 44. Cervical disc stimulation (provocation discography). In: Bogduk N, ed. Practice Guidelines: In Spinal diagnostic & treatment procedures. San Francisco: International Spine Intervention Society; 2004:95-111. 45. Franklin B. Poor Richard’s Almanack. Philadelphia. 1733. 46. Schellhas KP, Smith MD, Gundry CR, Pollei SR. Cervical discogenic pain. Prospective correlation of magnetic resonance imaging and discography in asymptomatic subjects and pain sufferers. Spine. 1996;21:300-312. 47. Grubb SA, Kelly CK. Cervical discography: Clinical implications from 12 years of experience. Spine. 2000;25:1382-1389. 48. Bogduk N, Aprill C. On the nature of neck pain, discography and cervical zygapophysial joint blocks. Pain. 1993;54:213-217. 49. Kambin P, Abda S, Kurpicki F. Intradiskal pressure and volume recording: Evaluation of normal and abnormal cervical disks. Clin Orthop Relat Res. 1980;146:144.

Discogenic Pain, Internal Disc Disruption, and Radicular Pain

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David G. Vivian, MM, BS, FAFMM

Discogenic pain (DP) and internal disc disruption (IDD) imply that the disc is the source of a patient’s spinal pain. As will be discussed further in this chapter, DP is a conceptual label that can be ascribed to a presentation of spinal pain but which cannot be verified by any known test. IDD is a specific entity that by definition pertains only to the lumbar discs and is diagnosed according to a tight protocol by provocation discography (PD). Both are diagnosed from a cohort of patients who present with nonspecific spinal pain (NSSP). Radicular pain is pain from a spinal nerve root. It is most commonly caused by disc prolapse and canal stenosis. It is far less common than NSSP and has a better natural history. Interventional management of NSSP is predicated on the ability to make a tissue-specific diagnosis, a process that requires the judicious use of interventional diagnostic techniques. This chapter concerns the diagnosis of spinal pain; diagnosis being the cornerstone of a doctor/patient relationship. Various spinal interventions will be discussed in following chapters. Each intervention requires particular knowledge and technical ability. Unfortunately, knowledge of the indications for these procedures and more importantly, their technical performance, have often fallen short of the mark—even in scientific publications.1,2 This has lead to a persistent skepticism about their efficacy. This fact is most evident in the development of radiofrequency neurotomy (RFN) treatments, and in subsequent meta-analyses and systematic reviews that gave equal credence to results, whether or not the technique was accurate.3

Social and Economic Dimension of Spinal Pain Low back pain (LBP) is a major health problem particularly in industrialized countries,4 affecting approximately 60% to 80% of the adult population at some stage5-7 and about 6% of people each day.6 LBP affects up to 80% of the working population during their lifetime and is the second most common reason for physician visits,8 and for work disability.9 Although LBP is typically self-limiting,10 it is still associated with substantial health care costs and absenteeism from work.4,11,12 Neck pain is also extremely common with a lifetime prevalence of 70%, a 1-year prevalence of 40%, and a point prevalence of 10% to 20%.13 Generalized musculoskeletal pain is also common: in one study of kitchen-hand workers it was present in 87%, and often present in multiple sites. In this study, neck pain was present in 71%, LBP in 50%, and forearm/hand pain in 49%;14 73% had pain in at least two sites, 36% in four or more, and 10% in

six to seven sites.14 In another study of 4006 workers from industrial and service companies, only 7.7% were free of regional pain of any description.15 In Australia, back problems are the most frequently seen musculoskeletal condition in general practice and the seventh most common reason for seeking care.16 In Australia, a 2001 survey found the point prevalence of LBP to be 26%, the 12-month prevalence 68%, and lifetime prevalence 79%.7 Only about 50% of the adult population experience low-intensity pain and low disability from it and another 11% experience high-intensity-pain but still low disability in a 6-month period.7 However, about 11% of the population experience high-disability LBP,7,17 and it is to this group that most resources are presumably directed. LBP is a costly problem. In early 2000, the cost of headache, LBP, arthritis and other muscle and joint pain to U.S. employers was more than $60 billion per year (these costs may have been underestimated because lost productivity among workers affected by a coworker’s diminished productivity was not taken into account).18 The majority of these costs (77%) related to reduced performance rather than work absence (workers who experienced lost productive time from a pain condition lost a mean of 4.6 hours/week). Workers who reported arthritis or LBP had mean lost productive times of 5.2 hours/week. It was established that these pains were directly associated with a 13% loss in productive time. Headache was the most common (5.4%) pain condition resulting in lost productive time. It was followed by LBP (3.2%), arthritis pain (2.0%), and other musculoskeletal pain (2.0%). Furthermore, the total health care expenditure only for LBP in the United States is even more alarming. When studied in 1998, total health care expenditures incurred by individuals with LBP in the United States reached $90.7 billion and total incremental expenditures attributable to LBP among these persons were approximately $26.3 billion. On average, individuals with LBP incurred health care expenditures at 60% higher than people ­without LBP.19 The lead researcher, Xuemei Luo, put these figures into the perspective of the U.S. economy by noting: “The total $90 billion spent in 1998 represented 1% of the U.S. Gross Domestic Product, and the $26 billion in direct back pain costs accounted for 2.5% of all health care expenditures for that year.” The largest proportion of direct medical costs for LBP is spent on physical therapy (17%) and inpatient services (17%), followed by pharmacy (13%) and primary care (13%).20 However, indirect costs, especially resulting from lost work productivity, outweigh other costs substantially.20 441

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Nonspecific Spinal Pain Nonspecific spinal pain (NSSP) is somatic referred pain derived from any spinal structure that is not associated with a specified “legitimate” or named condition. The issues for the clinician faced with a patient presenting with pain that appears to derive from the spine include (1) how to reliably determine that the pain indeed comes from the spine at all, (2) how to label the pain, (3) whether or not to try and make a tissue-specific diagnosis, and, if so, (4) how to make this tissue-specific diagnosis. Careful history and examination may at least be helpful in determining that the pain comes from the spine and whether or not it is caused by a red-flag condition. If clinical examination produces pain, it is likely that the pain derives from the spine. As a corollary, the absence of any painful restriction of movement on clinical examination should alert the clinician to the possibility of distant referred pain and such a negative finding is, in itself, a “red-flag sign”.21 Radiologic techniques are not helpful in resolving whether or not regional spinal pain originates from a spinal structure at all; imaging can exclude only red-flag or exotic causes of pain. Numerous studies on all imaging modalities used in the detection of morphologic changes in symptomatic and asymptomatic populations have failed to find significant differences that can be considered useful in any individual presentation of NSSP.22-46 Astoundingly, this well developed scientific fact has still not penetrated into standard health care practice; consequently, certainly the public and regrettably, some heath practitioners, remain misinformed about the relevance of technology as it applies to NSSP. The perceived contribution of the disc to spinal pain has been skewed by inappropriate use of labeling in the field of radiology.47 The label degenerative disc disease (DDD) pervades imaging reports and the scientific literature, yet there is no reasonable evidence to confirm DDD as being of any particular relevance to any single manifestation of NSSP. DDD is not a legitimate label for a patient with NSSP. The convenient and honest label to apply to otherwise unidentifiable somatic referred pain from the spine is the generic term NSSP, a label that means that the pain is derived from some unspecified site and related to some unspecified pathologic process. A label of NSSP means that for most patients presenting with somatic referred pain that appears to derive from a spinal structure there is no tissue or pathology-specific diagnosis. NSSP concentrates along the spine; early studies on pain referral patterns have shown that all of the innervated back structures can produce local pain with or without more distant referred pain.48-54 When the pain is concentrated in the lumbar spine, it can be called nonspecific low back pain (NSLBP); in the cervical region, it is called nonspecific neck pain (NSNP). These terms are synonymous and equally as useful as terms such as idiopathic back (or neck) pain and low back (or neck) pain of unknown origin. The pain experienced in NSSP is not necessarily confined to the region immediately adjacent to the spine, and it is this characteristic that provides the potential for errors in clinical judgment. The fact that NSSP can be associated with more distant referred pain (to the head particularly from the cervical spine, to the shoulder girdle and upper limb from the cervical and thoracic spines, to the chest and abdomen particularly from the thoracic spine, and to the lower limb from the lumbar spine and pelvis), has lead to mistaken management of many patients because it has often been assumed that NSSP in association with limb pain must be radicular

pain. Radicular pain is not the same as referred pain—and this single differentiation is perhaps the most important fact to elicit on clinical examination after red-flag conditions have been eliminated as a possibility. NSSP can be interpreted as being any pain that is thought to arise from an innervated somatic spinal structure where there is no substantive proof implicating any one structure. The label NSLBP means that the pain seems to come from some structure in the lumbar spine, and implies that there is no other information that can be simply gleaned to determine the source of this pain. On anatomic grounds, NSLBP could mean pain from one or more of any innervated structure, such as the discs, the zygapophyseal joints (ZJs), the sacroiliac joints, multifidus muscle, etc. However, as discussed earlier, NSLBP does not mean pain from disc or ZJ degeneration. When a patient presents with NSNP or NSLBP this is the diagnosis, even though it is semantically unsatisfactory, especially to the patient. However, such a label provides a good model for explanation of the possible pathology that might be causing or contributing to their pain. When a named condition is determined, it is removed from the general category, such as NSLBP, to a specific category, such as ZJ pain. For example, if a patient presents after a motor vehicle accident with somatic referred type neck pain spreading to the shoulder girdle and there are no red-flag conditions, the initial diagnosis is NSNP or one of its cogeners. If double-blind diagnostic blocks are used to diagnose or exclude say C2-3 ZJ pain in a patient presenting with suboccipital pain and headache after a motor vehicle accident, and the result is positive, then there is a high certainty that the diagnosis is C2-3 ZJ pain. Thus, the patient presenting initially with the general diagnosis of NSNP is then placed into a more structured subgroup, in this case ZJ pain, or more specifically, C2-3 ZJ pain, but only after the appropriate tests have been undertaken. The same could apply to DP if there was a valid test. A patient presenting with NSSP can be slotted into the subgroup of DP if it is considered that there is a diagnostic test used for DP that is accurate. It should be noted that medial branch blocks for the diagnosis of ZJ pain, and discography for the diagnosis of IDD, are currently the best tests for each condition, because diagnosis based on history, physical examination, and investigations, including MRI, have proved to be invalid and generally unreliable. As has been discussed, there is at this stage no test for DP. There is a test for IDD. A diagnosis of NSLBP is reasonable when a patient presents with, say, focal LBP with typical referred pain into the buttock and leg. One huge dilemma that has never been satisfactorily addressed is how to label the LBP component of a person who presents with widespread pain or pain in multiple sites, or how to label LBP if it is largely neuropathic in nature. Multiple pain sites might be present in a person with multiple injuries, but it also suggests a central pain processing process, and if so, it might suggest that tissue-specific diagnosis is likely to prove not helpful.

Referred Pain Referred pain can theoretically derive from any locally innervated spinal structure. The mechanism for referred pain is convergence.55 Somatic referred pain is pain evoked by the stimulation of the peripheral endings of nociceptive afferent fibers and is perceived in an ambiguous site due to the phenomenon of convergence when these afferents converge on second-order or third-order neurons in the central nervous system that happen also to receive afferents from the region to which the pain is referred.56 Under those

Discogenic Pain, Internal Disc Disruption, and Radicular Pain  443

conditions, and in the absence of additional sensory input to clarify the situation, the brain is unable to identify the source of the pain accurately, and attributes it erroneously to the entire area subtended by the common neurons.57,58 Ambiguity as to the source of information arises, either or both, because the painful structure is not densely innervated, and the central pathways along which the information is relayed are not highly organized somatotopically.59 NSSP is, therefore, different to radicular pain. Hence, lumbar ZJ pain,60 lumbar disc pain,61-63 and sacroiliac joint pain64 are described very differently to lumbar radicular pain. Information about referred pain from deep somatic structures has arisen from numerous important studies that identified the nature and spread of referred pain.48-54 Experiments on deep somatic referred pain by Kellgren52 in 1939 and Feinstein44 in 1954 showed that pain from deep somatic structures can be felt not only locally but also in distant areas; pain from deep lumbar structures refers into the legs as far as the feet; similarly pain from deep cervical structures refers into the arms and hands (Fig. 39-1). Later Hirsch and colleagues placed needles into various lumbar structures in people with LBP and reported that the disc was the most sensitive area for LBP.54 In this experiment, needles were placed into one or both of the lower two discs and into the ZJs, followed by the ligamentum flavum and the posterior ligamentous structures. When the disc was injected with 0.3 mL of saline a deep aching occurred across the low back. When the ZJ was injected, also with 0.3 mL saline,

the ache spread also into the buttocks and lateral hips. ­Additionally, deep somatic pain felt three dimensional; it was described typically as deep and aching, but other terms used included gripping, boring, crampy, and lumpy.48 Subsequently the pain from lumbar PD, in which intradiscal pressures probably rise above that used by Hirsch and colleagues, has been shown to be experienced as central low back pain that can also spread diffusely into the legs,65 and certainly below the knees.66 From these studies, various referral pain maps have been created, demonstrating that segmental referral patterns overlap substantially, and structures at one segmental level have similar pain referrals to other structures at the same level.67 Thus, although the site of pain may be a clue to a particular spinal segment, it is not a pointer to the specific anatomic origin of pain. From these studies, it is possible to construe that lumbar DP, or perhaps more specifically, lumbar IDD, is predominantly deep three-dimensional LBP that can spread diffusely into the legs. It is therefore possible to construct a clinical presentation that might be considered to be archetypal of, but not specific to, DP. Similar patterns exist in the cervical spine. Cervical ZJ pain, as ascertained by anesthetic blocks rather than provocation, extends beyond the local region to the ipsilateral occiput, shoulder and/or periscapular region (Fig. 39-2).67 Cervical disc pain, as ascertained by PD, can spread into the thoracic spine and the arms including the forearms, hands, and fingers.68-70 Cervical PD at any level produces local neck pain that is unilateral as often as it is bilateral,

Figure 39-1  Illustrations of referred pain patterns from injections of the interspinous ligaments with 6% saline using a 24 gauge needle. (From Feinstein B, Langton JB, Jameson RM, et al: Experiments on pain referred from deep somatic tissues. J Bone Joint Surg Am 1954;36-A:981-997.)

39

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with referral patterns as follows: C2-3 suboccipital and facial; C3-4 suboccipital, trapezius, anterior neck, face, shoulder, interscapular, and upper limb; C4-5 shoulder, interscapular, trapezius, extremity, face, chest and suboccipital; C5-6 trapezius, interscapular, suboccipital, anterior neck, chest and face; C6-7 interscapular, trapezius, shoulder, extremity and suboccipital; and C7-T1 interscapular (Fig. 39-3).71 Thus, cervical referred pain includes headache as well as arm, chest, shoulder, and thoracic pain.

Radicular Pain NSSP and radicular pain can extend to the limbs; it is therefore important to ascertain which type of pain is more likely because each must be considered differently from clinical and pathophysiologic perspectives (Fig. 39-4).72 Radicular pain is not the same as referred pain.74 Radicular pain is a particular type of neurogenic pain caused by direct injury to a sensory nerve root or dorsal root ganglion of a spinal nerve.74,75 Radicular pain is sometimes accompanied by objective signs of deficit or loss of neurologic function in a segmental distribution as a result of conduction block and it can coexist with spinal or somatic referred pain.74,75 Cervical radicular pain tends to be deep, severe, aching pain, and as such is different from lumbar radicular pain.74 Cervical radicular pain is experienced predominantly in the upper limb and shoulder girdle but when it occurs in the limb its distribution does not correspond to dermatomal maps of sensory deficit due to cervical radiculopathy.73 Cervical radicular pain from the C6, C7, and C8 nerve roots is felt in the arm with pain extending into the forearm and hand (Fig. 39-5).75 However, limb pain can also occur in referred pain, and because cervical radicular pain is uncommon, with an annual prevalence rate of 0.083% in one large population

C2-3

C3-4

C4-5

C5-6

C6-7

Figure 39-2  Zygapophyseal joint (ZJ) referral patterns: note that the C5-6 and C6-7 segments refer pain into the scapular region. (From Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint pain patterns. I: A study in normal volunteers. Spine 1990;15:453-457.)

study,76 deep aching arm pain is much more likely to be somatic referred pain than is cervical radicular pain. In contrast, lumbar radicular pain is classically an intense narrow band of lancinating, sometimes burning pain that refers down the limb, and often to the foot.77 The leg pain is typically more prominent than any LBP (indeed, LBP frequently is absent), and the leg pain tends to concentrate distally. Coughing, sneezing, straining at the toilet, and lifting will all classically exacerbate radicular pain, but such aggravating features are not specific to radicular pain. Pain is not limited to the dermatome and it may also be experienced in deep tissues innervated by the nerve.78

Concepts: Discogenic Pain, Internal Disc As at least the outer one third of the annulus fibrosus (AF) is innervated,79-81 the intervertebral disc is considered to be a possible source of pain that is otherwise labeled NSSP. There are five types of nerve terminations found in the lumbar disc: these have various morphologies and include simple and complex free nerve endings that concentrate particularly in the lateral disc, with a smaller amount posteriorly and the least amount anteriorly.79 Discogenic pain (DP) is pain that is considered to arise intrinsically from the disc. DP is frequently bandied about and assumed as a diagnosis, but the plain fact is that it is a diagnosis that cannot be substantiated. With the use of PD, the entity IDD has been defined according to specific diagnostic criteria.82 IDD is considered to be a subtype of DP.

Is There a Relationship Between Disc Degeneration and Discogenic Pain? Many published papers make the unsubstantiated statement that DD is a cause of NSSP. In fact, it has been clearly demonstrated that degeneration is not a term that can be used as a diagnosis of NSSP. Furthermore, the difference between aging and degeneration is not always clear; aging itself is not the major factor in the development of degeneration or spinal pain. Cellular function within the disc is mediated by at least five major factors: genetics, nutrition (diffusion of nutrients and oxygen across the disc matrix), cell function regulation (via IL-1, TNF-α, and TNF-β), age and senescence, and mechanical loading.83 The contribution to DD by genetic factors is highly significant; it may be as high as 80% in the cervical spine,84 and general heritability for DD ranges from 29% to 80% in different regions of the spine.84-86 In the lumbar spine, the genetic contribution is between 29% and 54%, with environmental influences of about equal importance.87 For example, smoking has a moderate influence on the prevalence of DD,87 presumably due to its effects on disc nutrition. This emphasizes that DD is not primarily or significantly caused by aging88 or by mechanically induced “wear and tear” processes.85,89 Studies with various imaging modalities on symptomatic and asymptomatic populations further emphasize that DD does not imply NSSP. In the cervical spine, radiologic DD is present in 13% of men and 5% of women during the third decade, in 85% to 90% of the population by the sixth decade, and nearly 100% by the age of 70 years.90 It occurs most commonly at C5-6, C6-7, and C4-5, respectively.42,91 In people aged 60 to 65 years without neck pain, about 95% of men and 70% of women have at least one degenerative change on their cervical spine plain radiographs.42 Lumbar degeneration, defined as a grade of ≥2 by the Kellgren-Lawrence scale; is present in Japanese females in 9.7% of the ≤ 39 age group, in 28.6%

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of those 40 to 49 years, in 41.7% of those 50 to 59 years, in 55.4% of those 60 to 69 years, in 75.1% of those 70 to 79 years, and 78.2% of those ≥ 80 years; and in Japanese males in 14.3% of the ≤ 39 age group, in 45.5% of those 40 to 49 years, in 72.9% of those 50 to 59 years, in 74.6% of those 60 to 69 years, in 85.3% of those 70 to 79  years, and 90.1% of those ≥ 80 years.92 Although plain radiographic changes, including vertebral end-plate changes, disc space narrowing, spondylolisthesis, spondylolysis, sacral lumbarization, wedge vertebra, a sagittal diameter of less than 12 mm and abnormal lumbar lordotic angle,44,93,94 have some predictive value for LBP, the relationship is mild at best,95 and their detection is largely

not helpful in the management of NSLBP because such changes occur frequently in the asymptomatic population.96 Although disc space narrowing at 2 or more levels from L1-2 to L4-5 shows the strongest radiologic relationship with LBP,97 similar comments apply. As a consequence, plain radiographs should not be ordered unless there is suspicion of a red-flag condition.98-101 The relevance of CT scanning is similar to plain radiographs; it is an excellent test for some red-flag conditions, demonstrates DD well, but it is not helpful in the detection of DP or ZJ pain. CT is better than MRI in detecting ZJ spondylitis,102 but this is of no particular clinical relevance. A newer technology, F-PET/CT (fluoride

A

B

C Figure 39-3  Illustrations of pain maps from cervical discography. A, C2-3 discogram pain referral map. B, C3-4 discogram pain referral map. C, C4-5 discogram pain referral map. Continued

39

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D

E

F Figure 39-3, cont’d  D, C5-6 discogram pain referral map. E, C6-7 discogram pain referral map. F, C7-T1 discogram pain referral map. (From Slipman CW, Plastaras C, Patel R, et al: Provocative cervical discography symptom mapping. Spine J 2005;5:381-388.)

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39

A

B Figure 39-4  A, Example of radicular pain (L5). B, Example of referred pain.

positron emission tomography with addition of CT) is more likely to be positive in symptomatic patients,103 but only time will tell if it has satisfactory validity in detecting a truly painful structure. Thus, there is no relationship between degeneration and NSSP and there is no demonstrable relationship between DD and DP.

Internal Disc Disruption and Discogenic Pain

A

B

The development of IDD as a concept emphasizes that abnormal morphology is not necessarily related to pain. IDD, a diagnosis that is defined by its diagnostic test, provocation PD, is pain perceived to arise from a disc that has undergone a specific type of degenerative process that is illustrated morphologically by radial tears in the AF. In addition, the diagnostic process recognizes that these changes may occur in the asymptomatic population, and as a consequence, clinicopathologic relationships only become evident when pain provocation or abolition is used to determine the painful from the painless disc. The degree of disc destruction itself is not a factor that can be relied on to delineate a structure causing a patient’s symptoms.

Diagnosis: Discogenic Pain and Internal Disc Disruption

C

D

Figure 39-5  Percent occurrence of symptom provocation per bit for C4 to C7 nerve roots. A, C4; B, C5; C, C6; D, C7.73 Note that the figures depict anterior and posterior views.

There are two possible methods that can be used to ascertain that a disc is a source of pain—namely PD and specific nerve block. If the nerve supply of the disc could be done efficiently it would establish a prima facie case for DP. However, the complexities of disc innervation may preclude such an eventuality. Nevertheless, some clinicians have made attempts.

The Diagnosis of Discogenic Pain Using Specific Nerve Blocks Lumbar discs are innervated by the lumbar sinuvertebral nerves, and branches of the lumbar ventral rami and gray rami communicantes (Fig. 39-6).104-106 The posterior and posterolateral portion of each lumbar disc is innervated by a branch of the ventral ramus

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Gray communicans block

Sinovertebral nerve block

Gray ramus communicans

Sinovertebral nerve L5

L5

L4 spinal nerve dorsal root ganglion

arising just lateral to the intervertebral foramen and by a branch of the gray ramus communicans just before it connects with the ventral ramus.106 The sinuvertebral nerves also innervate the posterior longitudinal ligament; the gray rami communicantes also innervate the lateral disc and the anterior longitudinal ligament,104,106 and in rats the DRG innervates other lumbar structures, such as, lamina, spinous process, back muscle fascia, and skin.107 The innervation by the gray rami communicantes is not a direct sympathetic innervation;106 it has been postulated that somatic and afferent fibers from lumbar structures use the gray rami as transmission pathways only.104,108,109 The rami communicantes branch from the spinal nerves just after they enter the intervertebral foramina, and then run anteriorly along the inferior third aspect of the vertebral body where they connect to the sympathetic trunk before branching to the lateral and anterolateral aspects of the discs above and below.104,110,111 The innervation of the disc might be blocked entirely by dual sinuvertebral nerve root blocks and sympathetic blocks. Sinuvertebral or nerve root blocks target the posterolateral innervation directly, but they are nonspecific because the spinal nerve and DRG are also blocked, and because epidural spread might produce further problems of interpretation. Various studies have been used to support or refute the utility of blocking the innervation of the disc.112-115 Although the nerve supply of the disc is nonspecific, if a local anesthetic block aimed at these nerves totally eradicated pain under controlled conditions, it might be possible to devise a treatment directed at the nerve similar to that performed for medial branch RF neurotomy. If this was the case, the interpretation would be that the pain was mediated by this particular nerve, not that the pain was necessarily discogenic.

The Diagnosis of Discogenic Pain or IDD Using Anesthetic Discography The disc itself can be blocked by intradiscal injection. Analgesic discography (AD) and functional analgesic discography are refinements of the technique of PD aimed at increasing the utility of

Figure 39-6  Innervation of the ­lumbar disc. Diagnostic and therapeutic injections, and thermal lesions, can target the sinuvertebral nerves and gray rami communicantes.

discography and, in particular, its specificity.116 However, the current definition of IDD does not include any statement about AD. There is no role for AD in discs with breaches through the outer lamellae (Dallas grade V) because pain reduction with leakage of any anesthetic agent into the epidural space could be a false-positive finding. This is the primary reason why there is at present no method for the diagnosis of DP in general; it is probable that discs with breaches in the outer lamellae can be a source of pain, but there is no valid method to make this connection. The problem with AD is that the anesthetic may not reach the painful radial tear owing to the dilution effect of contrast. If AD is to be used, it probably should be done directly via injection into the radial fissure.

The Diagnosis of IDD with Discography Although lumbar DP cannot be diagnosed using imaging, there is a significant relationship between disc morphology as determined by discography, and clinical pain as determined by the subjective provocation phase of PD. As a consequence, a particular cohort of otherwise labeled NSLBP patients can be defined as having IDD,117 a specific subtype of DP. Studies and reports on intradiscal therapies for putative DP have largely been drawn from patients diagnosed with IDD on the basis of PD. Discussion about the role and interpretation of PD can be found in Chapter 38. PD is used to confirm or deny the diagnosis of IDD, allowing for (1) enhanced ability to make a decision on interventional treatment—be it intradiscal therapy or spinal surgery; and (2) cessation of the search for other pain sources. The specificity of PD and, hence, the robustness of the diagnosis IDD has been questioned because of its propensity for false-positive findings.118-123 This can be minimized by careful patient selection; the risk of false positive findings is substantially diminished by selecting subjects with normal psychometric profiles who do not have pain in other regions.119,120 It would be folly to perform PD on a patient with fibromyalgia! The criteria for IDD are specifically applied to the lower lumbar spine (Table 39-1). There is insufficient

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Table 39-1  Eligibility Criteria for IDD Treatment Chronic, disabling NSLBP Failure to respond to noninvasive treatments No red-flag conditions No evidence of radicular or neuropathic pain No psychological barriers No greater than 25% loss of disc height Criteria for IDD by provocation discography satisfied IDD, internal disc disruption; NSLBP, nonspecific low back pain.

research on other areas of the spine to consider that intradiscal therapies have any traction in the cervical and thoracic spine for such regional NSSP presentations. In the cervical spine the disc cannot be pressurized because fissures are present in normal adult discs.124 Nevertheless, intradiscal therapies have been trialed in other regions. Discography arose because of its ability to detect morphologic changes in the disc that were not seen on other imaging techniques. However, the defining component of discography has been the pain response, not the morphologic changes alone. Clinicopathologic correlations have been found implicitly in IDD. The concept of IDD is supported by various biomedical features. Degenerative changes do not correlate with either positive pain response from discography or pain prevalence in general. ll Grade 3 fissures correlate strongly with pain, and are not related to age changes. ll IDD discs have abnormal stress profilometry:125 ll NP stresses are irregular and reduced, even to zero, whereas in normal discs there is uniform distribution of stress throughout all components. ll Posterior AF stresses are increased. ll Altered NP pressure can arise experimentally from end-plate fatigue failure,126 which has been demonstrated to occur with loads that are consistent with moderately heavy work activities.127 ll The biologic features of IDD have been reproduced in live animal experiments.128 ll The process of fibrosis is distinctly different in discs with IDD compared to control discs.129 ll

This last point is likely to be highly significant. The histology of discs that have been diagnosed with IDD using PD is different for discs in patients without LBP that have been assessed by PD as negative but degenerate on MRI and for cadaver discs that are macroscopically normal; the major difference is that in IDD there is a chronic inflammatory reaction with variable blood vessel infiltration.129 More specifically, the AF loses its normal lamellar structure, is disorganized and disrupted, and the fibers are cross-fused; the NP is markedly fibrosed, inflamed, and infiltrated with blood ­vessels.129 Additionally, immunohistochemical staining shows strong connective tissue growth factor (CTGF) expression in IDD discs, weak expression in asymptomatic DDs, and no expression in adjacent control discs in patients with IDD.129 CTGF is the downstream effector mediated by transforming growth factor-β1 (TGF-β1).130 CTGF is “closely associated with the regulation of cell proliferation and differentiation and the fibrosis

of tissues and organs, and can induce the in vivo expression of the gene involved with fibroblast extracellular matrix composition.”130 CTGF has a number of functions, one of which is the creation of some of the components of fibrosis by the production and accumulation of extracellular matrix.131 Healing of disc tissue is different to most other tissues because it is relatively avascular and takes place either from peripheral structures such as the outer AF and posterior longitudinal ligament,131 or via the end plate.132,133 Healing after injury to the AF or end plate is promoted and accompanied by vascular ingrowth, which stimulates vascular inflammatory reactions and the production of growth factors including TGF-β1 and CTGF.133 ­Aberrations of growth factor contribution to healing after injury to the AF or end plate are postulated to be a significant cause of DP. The validity of the diagnosis IDD is predicated first on the methodology of the PD, and second on patient selection for the procedure. The International Spine Interventional Society mandates the protocol as follows:82 (1) reproduction of the patient’s pain by stimulation of the affected disc; (2) such that the evoked pain has an intensity of at least 7 on a 10-point scale; and (3) pain is reproduced at a pressure of stimulation of < 15 psi; (4) provided that stimulation of adjacent discs does not reproduce pain; and (5) postdiscography CT demonstrates a grade III or IV fissure. That is, the disc is morphologically abnormal internally, but it is intact peripherally. A diagnosis of IDD can be made, therefore, on a disc that is normal on CT scan, and, dependent on the sensitivity of MRI, on a normal MRI.134 Patients with concordant pain at 15 to 50 psi might be labeled as having indeterminate pain, and those without pain until above 50 psi as definitely negative. Presumably, alterations in the pressure parameters used to diagnose IDD alter the robustness of PD to truly detect DP; however, this is a somewhat ethereal statement because there is no standardized criterion against which the concept of IDD can be tested. The features of IDD are characterized morphologically by: (1) degradation of the matrix of the NP, and (2) radial fissures, with or without a circumferential extension, that penetrate the AF without breaching the outer lamella. Fissures are graded on their extent, depending on whether they reach the inner, middle, or outer third of the AF,135 or if they extend circumferentially.136 The more extensive fissures that do not breach the outer lamellae of the AF correlate strongly with clinical pain and are associated with abnormal stress profilometry throughout the disc, including reduction and irregularity of NP stress, and increase in AF stress.125 ­Additionally, altered NP pressure can arise experimentally from end-plate fatigue failure,126 which has, in turn, been demonstrated to occur with loads that are consistent with moderately heavy work activities. Although it is likely that intrinsic DP can occur in discs that are disrupted to the point where the outer lamellae of the AF are breached (a grade 5 annular tear), it is not possible to determine that such a disc is the source of pain with PD (Fig. 39-7). On ­morphologic grounds alone, a discogram finding of a grade 5 disc disruption negates the diagnosis of IDD. On pain provocation grounds it is not possible to state that a disc with grade 5 change is the source of pain because of the high chance of invalid responses. If the outer lamellae are breached during discography, the provocation phase might not only produce a false-positive result because contrast and pressure is exerted into the epidural space, but also a false-negative response because the disc may not be able to be pressurized to the degree required by protocol or to a sufficient degree to reproduce the index pain.

39

450  Spine Grade I Radial fissure

Grade III Radial fissure

Grade II Radial fissure

Grade IV Circumferential fissure

Grade V Focal prolapse

established by discography, with sensitivity of 23.2%, specificity 96.8%, PPV 91.3%, and NPV 46.5% in one study.148 When Modic changes are studied according to type, the type 1 end plate has the highest PPV for positive PD at 81% (±7%).149 One of the problems of proton MRI is that the traditional T1 and T2 images measure the end stages of proteoglycan breakdown, by which stage water depletion is more severe. The earlier, more subtle, changes are not able to be detected with these sequences. As proteoglycans are highly negatively charged they attract cations, particularly Na+. Sodium MRI measures Na+ levels in the disc, thereby giving a direct measurement of proteoglycan levels. ­Depletion of Na+ is, therefore, a direct measure of degree of disc degeneration.152 Sodium MRI does not have the resolution of proton MRI, but it can now be studied as a potential surrogate for PD.

Can Clinical Tests Predict IDD?

Figure 39-7  The Dallas discogram description. (From Sachs BL, Vanharanta H, Spivey MA, et al: Dallas discogram description. A new classification of CT/ discography in low-back disorders. Spine 1987;12:287-294.)

How Useful Is MRI as a Predictor of IDD? As discussed earlier, MRI changes occur in the asymptomatic population,38,137, 138 and apart from the finding of a high intensity zone (HIZ) or Modic type 1 and 2 changes in the lumbar spine, the extent of changes are not predictive of the development or duration of future back pain.138 Attempts have been made to determine whether or not MRI can be used to predict PD outcome because PD is not without morbidity.139-141 Although MRI is somewhat predictive of a positive PD test when an HIZ or Modic type I or II changes are found, it is somewhat insensitive. The HIZ, defined on sagittal MRI as a very bright signal (equal to or brighter than CSF on T2-weighted scans) contained within the posterior AF,136 has been shown to have appreciable but variable correlation with positive PD in patients presenting with NSLBP.127 The initial study showed that an HIZ increases the odds that PD will be positive in that patient at that level by a factor of 6.5.136 Studies on the HIZ since that time have all shown that HIZ is highly specific (range 0.74 to 0.93)142-146 but that it has variable sensitivity, from as low as 0.09,146 to as high as 0.78.144 Thus, it is uncommon for an HIZ to occur in a disc that is not painful to PD, and the calculated likelihood ratios (ranging from 1.3 to 6.5 and averaging 4.1) indicate that an HIZ increases the odds that a PD will be positive by at least 50%.127 Additionally, although HIZs are present in both asymptomatic and symptomatic subjects, they are found significantly more in symptomatic (prevalence 60% ± 15%) than asymptomatic subjects (24% ± 11%).147 Modic changes have also been studied in relationship to NSLBP and PD.148,149 The overall rate of vertebral end-plate signal changes (VEPSC) is about 43% in patients with NSLBP and 6% in those without.150 The most common association of VEPSC and NSLBP is extensive Modic type 1 changes at L5-S1.151 Overall, ­VEPSCs are relatively insensitive, but quite specific, for the diagnosis of IDD

The prevalence of IDD in a population of NSLBP patients considered to be having sufficient pain and disability to undergo PD is about 35% to 40%.61,153 The prevalence of IDD in a group of patients with positive clinical indicators increases to 52% to 69%.153 The centralization phenomenon, or pain centralization, which is the retreat of referred pain toward the spinal midline during specified clinical examination, a history of persistent pain between acute episodes, a significant loss of extension, and a subjective report of so-named “vulnerability in the neutral zone” individually and in combination increase the likelihood of an eventual diagnosis of IDD in a group of highly disabled and psychosocially distressed patients with otherwise diagnosed NSLBP.153,154 ­Additionally, if vibration applied over individual spinous processes is considered a positive test, then the odds of a positive PD increases ­significantly.155,156 These clinical tests and protocols will need ­further validity and reliability studies before they can be considered to be adequate surrogates for PD.

The Diagnosis of Radicular Pain Due to a Contained Disc Prolapse The nature of radicular pain has been described. Apart from the description of pain, various clinical tests such as the straight leg raise test are used as aids to the diagnostic process, but their clinical utility is questionable,157 and radicular pain lends itself to imaging investigation. In the cervical spine, the neck compression, the axial manual traction test, and the shoulder abduction test are highly specific but poorly sensitive for the diagnosis of root compression.158 CT scan, MRI, and CT myelography can all be used in different clinical settings. If the morphologic findings match the clinical picture, then the cause of radicular pain can be assumed. The most common cause is some degree of disc prolapse. However, it should be noted that disc prolapse is also commonly seen in the asymptomatic population.34,36,41,159

Which Patients Should Be Considered for Intradiscal Therapies? Internal Disc Disruption and Discogenic Pain The patient with putative IDD or DP being considered for an intradiscal therapy should have had considerable NSLBP for at least 6 months. Each patient should have exhausted the options provided

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39

Four prerequisites for PD testing

Focal pain, with or without a component of referred pain

Little or no other pain in other areas of the body

Minimal disc space narrowing at the level to be treated

A fairly normal psychosocial profile

Figure 39-8  Ideal prerequisites if provocation discography (PD) is to be used as a test before an ­intradiscal procedure.

Figure 39-10  Illegitimate labels for a presentation of neck pain.

Figure 39-9  Cellular function within the disc is mediated by at least five major factors. (From Freemont AJ: The cellular pathobiology of the degenerate intervertebral disc and discogenic back pain. Rheumatology [Oxford] 2009;48:5-10.)

in less invasive care, and the pattern of pain should be such that it might reasonably be expected that the condition will not recover spontaneously. By the time a patient is being considered for PD, there is a reasonable chance that the pain and disability will be similar at 2 years, and perhaps improved by 5 years. The natural history of IDD over a 5-year period has been studied in a group of patients who elected not to have the subsequently offered posterolateral fusion surgery.160 In this study, 25 patients underwent PD after experiencing incapacitating NSLBP for a period of at least 6 months. The patients (n = 36) were selected from all patients who underwent PD (n = 432) over a 3-year period. Eligibility included single level PD positive (morphology and pain response), normal plain radiographs, and a minimum of 3-year follow-up. Of these, 25 patients were able to be studied, with average age at time of discography being 43 years, and at a mean follow-up time of 4.9 years, 68% had improved, 8% had stayed the same, and 24% were worse; 80% of those receiving worker’s compensation had improved. No patient had recovered fully. The natural history of IDD in a group of 36 patients undergoing placebo intradiscal injection over a 2-year period has also been documented by Peng and colleagues in their study on methylene blue.161 In this study, patients also had IDD using similar selection criteria but they elected to have the injection treatment. At 2 years the placebo group, with an average age of 42, had not undergone

much change in either disability or pain levels: there was a weak statistically insignificant trend to improvement of pain. The ideal patient has focal pain, with or without a component of referred pain, little or no other pain in other areas of the body, minimal disc space narrowing at the level to be treated, and a fairly normal psychosocial profile (Fig. 39-8). These are the ideal prerequisites in any case for a patient to be assessed with high quality PD that complies with recognized standards. If the PD is positive, the diagnosis of IDD (and thus DP) is then made (Figs. 39-8 through 39-10). The diagnosis of IDD does not imply that specific interventional treatment including surgery to the disc will produce good results.162,163 The cohort or cohorts of patients who might respond best to treatments arising from a diagnosis of IDD are still being defined. IDD can theoretically be treated directly by discectomy and fusion, discectomy and artificial disc replacement or by intradiscal therapies. The rationale for the first two procedures is that the painful structures within the disc are rendered pain free either by removal of the offending algogenic material and/or its immediate nerve supply, and the function of the disc is restored (artificial disc replacement) or made redundant (fusion). The rationales for intradiscal therapies include denervation of the offending tissue and improved tissue healing.

Radicular Pain due to Contained Disc Prolapse The patient with radicular pain due to a contained disc prolapse considered appropriate for an intradiscal therapy should have considerable pain that is not showing signs of recovery despite the passage of time and perhaps one or more epidural injections. This can be a hard situation to call. Also, if such a therapy is suggested, the clinician should be able to justify using an intradiscal treatment over minimally invasive treatments including minimally invasive spinal surgery.

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Surgery for radicular pain caused by a disc protrusion has been considered successful for many years since the discovery of the disc prolapse and its effects on the neural system.164 It is instructive to consider that the natural history for radicular pain due to disc prolapse is reasonably good in any case,165-168 and surgery has proved popular not necessarily because of its better long-term outcome,169 but because it provides the quickest route to recovery.165-169 Surgery may be superior to conservative care within 12 months but by 4 years there is no difference in outcome.170 Large disc protrusions or extrusions treated conservatively for the presentation of radicular pain do resolve when followed with imaging techniques: smaller protrusions tend not to resolve.171 Once a decision is made to perform an invasive technique, any outcome that seems to be predicated on bony canal dimension reduction demands spinal surgery. Intradiscal decompression is for contained and, therefore, small disc protrusions that are not recovering quickly enough.

Which Patients Should Not Be Considered for Intradiscal Therapies? Purely on face validity grounds, the more that the presenting pain is localized into one region, the more likely that it is derived from a local structure. As a corollary, chronic widespread pain, which is present in about 4.5% of the population,172 could derive from multiple regions or from an underlying pain dysfunction, such as central sensitization. There are schools of thought postulating that most, if not all, chronic NSSP is caused by central nervous system processing dysfunction independent of any initiating musculoskeletal event. Fibromyalgia (FM), the most common known cause of chronic, widespread pain,173 is an example of a presentation that could mimic DP. It is considered to be present in between 0.5% and 7% of the population at any given time.174-176 It is not uncommon for a patient, who presents to a spinal clinic with a pain diagram demonstrating only focal LBP, to reveal under closer questioning a profile consistent with FM. Additionally, there are others who present somewhere short of the FM diagnostic requirements.177 They might get labeled with an entity such as diffuse myofascial pain. The essence is that they do not have relatively focal regional pain like that described earlier for focal deep somatic pain referral, and they might have some of the accompanying symptoms of FM, such as sleep disturbance, unrefreshed sleep, and general autonomic symptoms. Local neuropathic pain should also alert the clinician to be wary. Neuropathic pain can be challenging to diagnose because diagnostic criteria are still developing, and neuropathic pain can manifest simultaneously with somatic referred or other pain.178 The diagnosis of neuropathic pain is based primarily on history and physical examination.179 Although neuropathic pain can have deep aching and shooting characteristics, more typical of lumbar radicular pain,75 it also attracts other descriptors such as burning, crushing, punishing, and cruel,179 and it can be associated with abnormal sensations such as formication. Because it is often unrecognized by clinicians,180 a range of neuropathic questionnaires, such as StEP,181 PainDETECT,182 DN4,183,184 LANSS185 and NPS186 have been developed and reviewed.187 The prevalence of neuropathic pain in the general population is about 7% of which 70% have pain in the moderate to severe range.188 Additionally, although some of these questionnaires should be considered

a screening tool only and population surveys should be treated with some scepticism,189 one survey report using PainDETECT found that the prevalence of predominantly neuropathic pain in a population of people with LBP was 37%.182 In an orthopedic setting of patients with predominantly LBP, those with a positive PainDETECT questionnaire had a median VAS of 5.0, and some had features typically representative of radicular pain and/or radiculopathy, including typical radicular pain (40%), positive Laségue sign (18%), or absent reflex (17%).190 More than two neuropathic pain characteristics were present in 34% of these patients. Although neuropathic pain may represent radicular pain, it is fair to say that when a person presents with LBP that has neuropathic descriptors rather than deep somatic pain descriptors, clinicians should consider that the pain is more complex than being simply derived from a local somatic structure such as a disc. Pain centralization may be a significant factor. The patient with significant psychological features in association with pain is difficult to assess from a pain origin perspective. Although it has been reported that alleviation of pain from a surgical procedure can return abnormal psychological parameters to normal,191 the false-positive rate of interventional diagnostic tests such as discography is an example of the difficulty in assessing such a presentation.120 In summary, the presentation that might lead a clinician to the suspicion of deep somatic referred pain from a disc is that of deep aching pain that is localized predominantly in one region of the spine with or without referred pain from that region into the limbs or trunk, without any substantial abnormality of psychological profile, perhaps other than distress. The presentation that might lead to the opposite conclusion is when the pain is more widespread or has prominent neuropathic qualities suggestive of radicular pain or central sensitization pain, or if the psychological profile is substantially abnormal.

Why Is There Such A Problem with NSSP? The essence of tissue-specific spinal pain diagnosis is that it requires the use of invasive special tests such as medial branch blocks and discography. These tests should be performed only when they serve some use. They should be performed when a useful tissue-specific treatment is planned. For the majority of patients presenting with spinal pain these tests are unwarranted because the condition can be dealt with in a less invasive manner or because there is no valid treatment. When a person presents with spinal pain, the initial aims are to ensure that the pain derives from the spine and that it is not caused by any red-flag condition. The next aim for the clinician is to use the available evidence to guide treatment. There is some good evidence about prevention of LBP chronicity, and this should be used where applicable when a diagnosis of NSLBP is made. As will be discussed, the use of fear-avoidance and “move it or lose it” type models have excellent evidence for prevention of this chronicity, at least for NSLBP. Despite this, evidence has not been converted into practice. Specific traditional treatments have not proved effective in controlling the epidemic of back pain. Because about 70% of the acute back pain population recovers rapidly, therapies that are no better than placebo have been ascribed healing properties they do not deserve. The challenges for those who manage back pain are to provide a management strategy that actually alters the long-term outcome and to identify, if possible, and as early as possible, the patients who are less likely to recover.

Discogenic Pain, Internal Disc Disruption, and Radicular Pain  453

To this end, a number of evidence-based guidelines for the clinical management of acute back pain in primary care have been developed.192-199 In general, the guidelines subscribe to the concept that exercise is beneficial, fear of movement is harmful, that consequent pain should not be understood to be further injury, and that chronicity is contributed to by avoidance of these concepts. More specifically, they (1) identify potentially serious causes of acute low back pain (< 5%); (2) promote effective self-management of symptoms through the provision of timely and appropriate advice; and (3) maximize functional status and minimize disability. A multidimensional approach is required to translate these concepts into reality for the public and the medical profession.200,201 One way to promulgate the guideline concepts is with mass-media campaigns, which have been shown to be effective in delivering health information to medical and allied health practitioners and the general public,202,203 although the effective penetration relates more to public perception changes than alterations in the attitudes or behaviors of health professionals.204 A mass media campaign that outlined some evidence-based facts about back pain was implemented205 and was found to be useful.206,207 The campaign issued sharply focused, unambiguous advice directed toward staying active and exercising, not resting for prolonged periods, and remaining at work.208-211 Such programs do not necessarily translate into huge savings.210 Guidelines in general do not lead to improvement of clinical outcomes, primarily because they are not followed by practitioners.210,212-218 Reasons for this include poor penetration of clinical guidelines into graduate and postgraduate medical education, lack of awareness, inability to understand the ramifications of referred pain, lack of commitment to change, incomplete understanding of the natural history of LBP, disagreement with evidence-based recommendations, concern for litigation, a belief that guidelines cannot be adequately explained to patients and particularly lack of uniformity in management by the various health professionals.212,218-222 It is also not easy to remedy lack of compliance to guidelines.210,220,223 It is apparent that the proper use of clinical guidelines in the management of LBP produces better outcomes.224-226 Guidelines tend to portray LBP as a benign, self-limiting disease, as single attacks tend to recover.227 Consequently it is not surprising that some primary care practitioners adopt a blasé attitude to an acute presentation of LBP, despite evidence clearly demonstrating that early diagnosis and suitable advice underpins the long-term outcome for many patients.224 The end result of lack of compliance to guidelines is prolonged unnecessary disability and increased usage of the health-care system. For example, a survey on the usage of the health care system over a 12-month period in a longitudinal prospective cohort study following presentation with LBP revealed alarming data.227 Of the 1342 patients, 57% were seeking additional specialist care, 46% had some form of imaging, 49% underwent physiotherapy, and 31% received massage. Because specialist care resulted in more imaging and intervention, it was considered that a significant contribution to the problem was the lack of a well-functioning primary care gatekeeping force.227 So, one problem is the dissemination and utilization of evidence-based clinical guidelines to those practitioners in the front line of LBP management. Promoting adherence to LBP guidelines requires more than enhancing knowledge about its evidence-based management.212 Public education and an interdisciplinary consensus are important requirements for successful guideline implementation into daily practice.212 Guideline recommendations need to be

adapted to the infrastructure of the health care system in general.212 Most guidelines refer to the management of LBP in general. However, in respect to work-related acute LBP, specific guidelines do exist.228-230 In the first instance, we need to know if these guidelines are of sufficient quality on which to base the management of LBP.

Preventative Measures There are two important studies that emphasize the benefits of early assessment and active management of acute LBP. In Indahl’s study,225-226 in which workers with LBP were put into one of two groups and followed up for 5 years, 19% of the patients in the intervention group, compared with 34% in the control group, were still on sick leave after 5 years. The successfully treated group was managed with an approach that included clinical examination combined with information for patients about the nature of the problem provided in a manner designed to reduce fear and give them reason to resume light activity. It might be reasonably assumed that Indahl was able to successfully rehabilitate the 15% of people who had a reversible primary psychosocial reason for nonrecovery of function, and that the other 19% who remained disabled had significant underlying pathologic processes or some other unknown factor responsible for this disability. Evidence-based care has been further studied. A seminal study on WorkCover patients which offered these workers a choice between Indahl’s evidence-based care and usual care (e.g., from the family general practitioner) in four district hospitals in Newcastle, Australia, also showed the benefit of early decisive management of LBP.224 In this study, the 65% who accepted evidence-based care were compared to the other group. The specialist in this clinic practiced according to Australian Evidence-Based Guidelines for Management of Acute LBP.198 These guidelines are similar to other published guidelines except that they do not use treatment by manual therapy, a treatment that seems to lack significant positive evidence.231 The emphasis is on explanation, reassurance, encouragement to remain at work, simple analgesics, avoidance of passive therapies, and worksite visit/intervention if indicated. Imaging was performed only if there was a clinical red-flag indicator. Instructions on how to implement these guidelines have been discussed in detail.232 In this study, the physician saw the injured worker at the hospital clinic, often on the day and virtually always within 48 hours of injury. At consultation, clinical examination consisted of history of the injury, past history, red-flag checklist, and examination. Management was by explanation of the benign nature of LBP and of its good prognosis. Fears or misconceptions that the patient had were identified and addressed. Workers were specifically reassured on the basis of evidence that a good outcome was highly likely and were encouraged to remain at work. They were given simple analgesics particularly paracetamol and simple McKenzie type stretching exercises. If the worker had any occupational safety issues at work, that was further assessed. The patients were reviewed at 1 week. This study followed 253 patients. Of these, 62 elected usual care (private general practitioner, etc.), 191 (75%) consulted the staff specialist (of these, 27 [14%] elected to change to usual care after the initial consultation), and 164 (65%) remained under the care of the staff specialist. The outcomes are summarized in Table 39-2. A group of 84 patients who saw the staff specialist were identified as having credible back pain but alleged disability dissonant with the history of injury. Psychosocial factors in this subgroup included job dissatisfaction or dislike of the supervisor. Of these 84 patients,

39

454  Spine

Table 39-2  Outcomes of Workers Presenting with Acute Back Pain Evidence-Based Care (%) Immediately back to normal duties Modified duties

Usual Care (%)

63

0

37

92

One person

35

Percentage fully recovered

98

84

Recurrence

6

27

Time off work

From McGuirk B, Bogduk N: Evidence-based care for low back pain in workers eligible for compensation. Occup Med [Lond.] 2007;57:36-42.

13 transferred to usual care but 71 remained under evidence-based care. Although they required a longer initial consultation and a greater number of consultations, their outcomes were favorable and did not statistically differ from other patients who pursued evidence-based care. Additionally, of the entire group, 32% accepted evidence-based care readily, 24% came to the consultation with preconceived beliefs about back pain management, and 44% expressed job dissatisfaction and psychosocial difficulties in the workplace. When evidence-based care was explained, most of the group with preconceived beliefs accepted evidence-based care. Patients with psychosocial difficulties required more consultations and care, but ultimately had similar outcomes as the rest. Only 14% declined the option of evidence-based care. Workers under evidence-based care achieved outcomes that were statistically and clinically better than those achieved under usual care, in particular for return to normal duties, lost time, recovery, and recurrence. Furthermore, early intervention with evidence-based care was associated with a high rate of full recovery and low rates of recurrence and chronicity. Where necessary, worksite intervention was a critical component of management. This included ergonomic and safety issues and extended to resolving psychosocial issues in the workplace.

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Intradiscal and Peridiscal Therapies for Discogenic and Radicular Pain

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David G. Vivian, MM, BS, FAFMM

Intradiscal therapies are those that involve the placement under imaging guidance of a needle, probe, or similar device into an intervertebral disc with the goal to reduce the patient’s presenting symptoms. Chemonucleolysis, a term coined by Smith and Garvin in 1963 when they injected chymopapain into a disc for the treatment of sciatica,1 was the first intradiscal therapy; it was designed as a minimally invasive treatment for radicular pain caused by a disc prolapse. Chymopapain was eventually shown to be an extremely effective treatment, but ironically ceased to exist mainly for political reasons. However, the main thrust on epidemiologic grounds has been the search for a minimally invasive panacea for spinal origin pain, particularly nonspecific low back pain (NSLBP). As a consequence, numerous device companies have developed experimental intradiscal devices, some of which have achieved modest success in the small cohort of patients who present with NSLBP and are given the questionable diagnosis of discogenic pain (DP). Most research into a minimally invasive remedy for DP has involved intradiscal thermal therapy. Unfortunately, there have been two major drawbacks in this development; firstl, there is no clarity as to what constitutes DP, and second, the perceived mechanisms by which intradiscal thermal therapy might be incorrect. DP is a theoretical concept in which the premise is that a patient’s pain is derived intrinsically from the disc. DP remains conceptual because it is a diagnosis that cannot be established with current know-how and technology. It was hoped that tests such as spinal MRI, with its spectacular ability to demonstrate morphologic changes, would be the definitive test that established a diagnosis of DP in a patient with nonspecific spinal pain. Unfortunately, MRI has not helped in this regard. Given that DP cannot be diagnosed on clinical examination and with the aid of special tests, the issue remains that there is still a need in some instances to find a treatable solution for a presentation of nonspecific spinal pain (NSSP) that might arise intrinsically from the disc. The two methods used to establish whether a particular structure is a source of pain are pain provocation and pain blocking. Provocation discography (PD) has been used as the method for establishing the possibility of DP; the provocation component seeks to establish if the patient’s pain is reproduced, and further, with the addition of contrast it can be determined if the internal structure of the disc is consistent with one that might lead to DP. Pain blocking has not been used to any significant extent in determining if the disc is the source of pain. However, in recognition of the lack

of specificity of pain provocation, recent innovations in discography include the addition of a postprovocation phase in which the disc is injected with anesthetic in an attempt to abolish or reduce the patient’s pain. This method has not proved to be more decisive, however. The alternative method that can theoretically be used to establish the disc as a source of pain is to block the nerve supply to the disc, but this technique is technically difficult, most likely imprecise, and lacks specificity. The diagnosis established by provocation discography (PD) is internal disc disruption (IDD). In IDD, the disc is shown to be internally disrupted and the probable source of pain, and it is thought that the radial fissures are the prime source of pain. The credibility of the diagnosis IDD is dependent on the validity and reliability of discography. The diagnostic confidence of IDD can be manipulated by altering the criteria for calling a PD test as positive. Indeed, over the years these criteria have changed and it may be that they will change in the future. Initially discography was deemed positive when internal disruption was seen, but when morphologic change alone was shown to be nonspecific, pain provocation was added. With the recognition that pain provocation was itself nonspecific, the nature of pain provocation was redefined so that pain had to (1) reach a minimum intensity (currently about 7/10 on a VAS); (2) be exactly like the clinical pain; and (3) not be produced at adjacent discs The Diagnostic Criteria for IDD from the International Spine Intervention Society (ISIS) are presented in Table 40-1.2 It may be that further refinements of discography will increase the confidence that IDD is a credible diagnosis. If it is, then diagnosis should lead to a predictable outcome for this cohort, be it with conservative or interventional management. Another problem in this area of medicine is proving treatment efficacy. The future development of treatments for IDD is likely to be constrained at least because of the costs of running multiple randomized controlled double-blind trials (RCDBTs). The estimated cost of a previous intradiscal electrothermal study was estimated to be more than $1,000,000.3 An alternative is to use well designed, properly conducted observational studies as the benchmarks that establish whether a particular procedure is backed by a suitable level of evidence of efficacy.3 Such studies are particularly good in at least refuting ineffective procedures and practices.3 The recent publication of the first RCDBT on MB suggests that it is an extremely effective treatment for IDD.4 Other studies are underway to further assess this treatment. 461

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Table 40-1  Diagnostic Criteria for IDD from ISIS (2004)*

IDET: IntraDiscal ElectroThermal Treatment

1. Reproduction of the patient’s pain by stimulation of the affected disc 2. This pain must have an intensity of at least 7 on a 10-point scale 3. This pain must be reproduced at a low pressure of stimulation: 15 psi (1 kg cm2) 4. Stimulation of adjacent disc(s) must not reproduce pain 5. Postdiscography CT demonstrates a grade III or IV fissure *All

categories must be satisfied. These criteria are being modified. IDD, internal disc disruption; ISIS, International Spine Intervention Society. (From International Spinal Intervention Society. Lumbar disc stimulation. In Bogduk N (ed): Practice Guidelines for Spinal Diagnostic and Treatment Procedures. ­International Spinal Intervention Society, San Francisco, 2004, pp 20-46.)

Intradiscal Thermal Therapies for Discogenic Pain Intradiscal therapies for DP, and more specifically for IDD, are not standard treatments. They are in development. Bogduk has enunciated the status of intradiscal procedures elegantly as follows:5 Where I and the colleagues in my department differ from most other practitioners is the context in which we provide intradiscal therapy. We do so only with the approval of an ethics committee. The terms of approval allow us to evaluate the efficacy of such interventions and the efficacy of adaptations, such as multiple placements of electrodes, designed to improve efficacy. In consideration of this approval we undertake to monitor and report our outcomes. Under these conditions we invite patients to participate in studies of emerging technology. That way we offer them the possible benefit of these procedures without pretending that they will work.

Types and Methods Discogenic and radicular pain can be treated with thermal intradiscal procedures (TIPs) that typically use radiofrequency (RF) energy delivered into the disc by a locally placed probe or similar device aimed at altering disc structure, removing disc tissue, or denervating nerves. Other patented energy sources that can be used include thermal, electric current, microwave emission, ultrasound emission, radioactive emission, and laser. Although RF is the most commonly used energy source, ultrasound is at least as good.6 RF technology has been used since at least 1891 when D’Arsonval used alternating current to prevent any unwanted effect of neuromuscular stimulation during surgery. Subsequently, Harvey Gushing developed the technique of high-frequency current for electrocoagulation of blood vessels during surgery.7 It was subsequently shown that high frequency lesions in the RF range were reproducible and well defined.8 Since this time, the technology has advanced, and RF current is used in multiple arenas, including neurosurgery, dermatology, chronic pain, and in the treatment of cardiac arrhythmias. The three minimally invasive TIPs for the treatment of IDD are intradiscal electrothermal therapy (IDET), percutaneous intradiscal radiofrequency thermocoagulation (PIRFT), and intradiscal biacuplasty. The generic name given when any of these three methods are applied to the AF is annuloplasty. PIRFT has also been applied into the NP. The TIPs used to remove or ablate disc material and thus decompress the disc include percutaneous lumbar discectomy,

5-cm active tip in circumferential fissure Figure 40-1  Schematic representation of IDET with the lesion seemingly applied across the radial tear.

laser discectomy, and disc decompression using RF energy (DISC nucleoplasty). Intradiscal electrothermal annuloplasty (IDET) uses the Smith and Nephew Endoscopy (Andover, MA) SpineCath System in which a navigable catheter with an embedded thermal resistive coil is inserted posterolaterally into the AF. The catheter is then advanced through the disc circumferentially to return posteriorly. With the use of indirect radiofrequency energy, electrothermal heat is then generated with the thermal resistive coil; the disc material is heated for up to 20 minutes to 90° C (Fig. 40-1). Percutaneous intradiscal radiofrequency thermocoagulation (PIRFT) differs from the IDET procedure in that radiofrequency energy is applied directly to the involved disc, either into the NP or the AF (DiscTRODE; Radionics, Burlington, MA). Intradiscal biacuplasty (Baylis Medical, Montreal, Canada), uses RF energy directly to heat the AF while circulating water is used to cool the tissue that is adjacent to the needle. Two probes are placed on the posterolateral sides of the AF through introducer needles and the disc is heated by RF waves. The electrode surfaces are cooled by circulating water in the electrodes, thereby heating the disc tissue to 45 to 55° C—a temperature range that is considered to be neurotoxic.9-11 In fact, this technique can produce temperatures in the 46° to 67° C range in the inner two thirds of the AF, more than 45° C in the outer third and less than 42° C in the cauda equina,12 thus supporting other evidence that at least the procedure is safe13 (Fig. 40-2).

Heat Lesions: Extent and Effect IDET and other thermal treatments were developed to produce intradiscal temperatures sufficient to at least ablate AF nerve fibers and also to denature AF collagen. RF lesions on peripheral nerves in dogs showed that at up to 6 weeks, there was a total loss of unmyelinated and a near total loss of myelinated fibers with lesions at temperatures as low as 45° C.14 This figure has not been verified in humans. It was considered that for denervation to occur, intradiscal lesions had to be above 45° C, but it may be that a significantly higher temperature is required. Safety was ensured by keeping

Intradiscal and Peridiscal Therapies for Discogenic and Radicular Pain  463

Figure 40-2  Disc biacuplasty.

temperatures in adjacent tissues below certain tolerance levels. Spinal cord and nerve root ischemia can be prevented by observing that the maximum tolerable temperatures in the CNS are 42.0 to 42.5° C for 40 to60 minutes and 43° C for 10 to 30 minutes.15 It had also been observed that collagen denaturation, from a triple helix to a random coil with variable crosslinking,16 occurred in other tissues at 60° -65° C.17,18 It was noted that this effect produced stiffening in shoulder capsule and tendons, leading to stabilization, as well as subsequent beneficial biologically mediated effects including increased strength; the process was accompanied by histologic changes, such as degradation and replacement of collagen fibrils, and signs of healing including increased cellularity, reactive fibroblasts, and increased vascularization.19 Thus, it was considered that thermal lesions in the disc could achieve collagen denaturation and denervation by producing intradiscal temperatures up to 65° C providing that surrounding structures were not heated beyond tolerance levels. Subsequent cadaver experiments indicated that the temperatures developed by IDET could reach 60° C or more up to 2 mm from the catheter, 60° C between 2 mm and 4 mm away; and 45° C 9 mm to 14 mm away.20 It is notable that the region of increased temperature around IDET is small.16,20It was later reported that the temperatures reached in the AF by IDET were independent of the degree of DD,21 always reached 45° C, but did not always reach 60° C.21 Experimental Methods and Effects Some of the cadaveric studies on thermal intradiscal thermal lesions have obvious limitations, not the least being their inability to model short- and long-term tissue responses to trauma.22-25 Live animal models also suffer because they address morphologic changes and not pain responses. The most significant finding from these studies is that, perhaps consistent with morphologic differences between disc and shoulder capsule, the same process of stiffening does not occur in the in vivo animal disc;26-28 heat does not cause acute or chronic stiffening of the healthy disc.19,29 The first change that occurs after the introduction of any device within the disc is the development of fibrosis.30

There is no healing response.19 For example, at 12 weeks after disc incision, there is proteoglycan death, vascular granulation tissue consistent with an attempt at a healing response extending to one third of the AF depth, with grade 3 or 4 DD (Gries classification),31 and sparse neoinnervation in the outer AF. As an aside, it is notable that these changes do not necessarily occur with AF stab incision needles with a 19 gauge needle.21 The higher the temperature, the greater the AF destruction.21,26,32,33 Bass and colleagues performed an in vivo study, with animal sacrifice at 7, 45, or 180 days, on ovine cervical discs, demonstrating that high temperature treatment (70° C for 10 minutes) causes AF tissue degradation, but lower temperature lesions (52° to 54° C) have minimal adverse biomechanical effects compared to sham treatment.19 The most outstanding feature of intradiscal heat is it causes progressive deterioration of disc morphology without any healing response.19,21 Thus, the process is very different to that seen in joint capsule and tendon. It is also unlikely that IDET lesions have an effect by denervation. It is theoretically possible that reinnervation of the NP is a significant mechanism for DP. Freemont and coworkers demonstrated a propensity for patients with IDD having fusion for LBP to develop reinnervation into the inner third of the AF (46%) and NP (22%), but also noted that these changes occurred but to a moderately lesser degree in nonpainful disc samples,34 a feature also noted in severely degenerated discs in any case.35 But do these thermal lesions actually denervate the disc? The heat required to produce denervation in peripheral nerves is at least 45° C.36 ­However, when IDET at 90° C was performed in sheep with experimentally induced posterolateral AF lesions with temperatures in the adjacent AF tissue raised to a mean of 63.6° C and in the NP of 67° C, there was not only a lack of tissue repair, but also a lack of denervation.21

Efficacy of Intradiscal Electrothermal Therapy Intradiscal electrothermal therapy (IDET) is, by far, the most studied intradiscal therapy. Studies on IDET have been confined to the treatment of IDD. IDET has not been tested on other cohorts, such as patients with NSLBP who, for example, have DP diagnosed with nerve blocks or on patients with MRI-detected morphologic changes. It has also not been studied to any significant extent on other areas of the spine. As IDET targets fissures in the peripheral AF, it is logical that it should only be performed if the cause of pain is in the peripheral AF. The detection of annular fissures is one of a number of criteria for IDD.37 IDET is a technically demanding procedure. It requires precision: the lesion must be placed in the outer zone of the AF or across a radial fissure. IDET creates a small lesion (a few mm); even if the lesion seems well placed in axial views, it may be that in the horizontal dimension the lesion is applied above or below the painful fissure (Fig. 40-3).23 Additionally, if IDET works by neurotomy, the IDET lesion must be large enough to coagulate a critical number of nerve endings to produce pain relief:23 perhaps such widespread denervation is not achievable. IDET has been found to, at best, benefit only a small cohort of patients with IDD and at worst to have no efficacy. The more important studies on IDET are on patients with IDD as determined by the strict ISIS criteria. In these studies, IDET has been performed optimally, with electrodes placed as far posteriorly in the AF as is feasible.23 Small lesions directed at poor targets should be no better than placebo!

40

464  Spine

Lesion Lesion

Annular tear Annular tear

The evidence about IDET derives primarily from two controlled trials on IDET using sham procedures as the control,38,39 and one prospective cohort study using patients denied interventional treatment as a comparison group.40,41 Although the Bogduk40,41and Pauza39 studies showed a number needed to treat (NNT) of five for excellent pain relief with the use of IDET, the Freeman42 study showed no benefit over placebo. Secondary information has been obtained from numerous observational case series.43-64 All of these studies, with the exception of one that did not record the device,46 used the SpineCATH. From these studies six systematic reviews have arisen.65-70 Group data from these observational studies show, in general, modest but definite improvements in pain and function,43,46,50,51,56,58,61,79, and these results seem to be much the same as might be expected from other interventional treatments including spinal fusion for the management of IDD. Reported outcomes have generally been the same for compensation versus noncompensation cases.40,41,47,80,81 There have been numerous systematic reviews that contain comments on IDET.65,66,70,84, Derby and associates consider that IDET provides a cheaper, less invasive, and safer alternative than does spinal surgery for the treatment of IDD—especially in patients with less functional impairment, relatively well maintained disc heights, and DP caused by annular tears or protrusions less that 3 to 4 mm.82 Derby further commented that of six IDET studies with sufficient reported data,39,40,46,52,85 between 38% and 94% (average 71%) of patients reported greater than 50% of pain relief 6 to 24 months after IDET.82 Overall, the success rates for IDET are modest. This may reflect the fact that IDET is a technically demanding procedure. It requires precision: the lesion must be placed in the outer zone of the AF or across a radial fissure, and even if on an optimal position, it creates only a small lesion (a few mm). Even if the lesion seems well placed in axial views, it may be that in the horizontal dimension the lesion is applied above or below the painful fissure.23 Additionally, if IDET works by neurotomy, the IDET lesion must be large enough to coagulate a critical number of nerve endings to produce pain relief:23 perhaps such widespread denervation is not achievable. Randomized Controlled Studies on IDET Pauza found 1360 eligible patients after a telephone interview, and, after performing discography on 260 of them, found 64 who met the criteria for IDD using pressure-controlled PD.39 Patients were treated with IDET or sham IDET, with the catheters in excellent position, and were followed for 6 months. The mean pretreatment

Figure 40-3  Schematic representation of an IDET lesion placed above a radial tear. IDET, IntraDiscal ElectroThermal treatment.

VAS was 6.6 in the IDET group and 6.5 in the control group, and at 6 months, the improvement in VAS for IDET was 2.4 versus 1.1 in the control group. There was also a significant improvement of physical function in disabled patients and a trend to improvement in SF-36 Bodily Pain subscale. Approximately 40% of patients experienced greater than or equal to 50% pain relief, and approximately one out of five experienced greater than or equal to 75% pain relief. Freeman performed a prospective, randomized, double-blind, placebo-controlled trial of IDET comparing this treatment group with a sham procedure for the treatment of chronic discogenic low back pain. Inclusion criteria included the presence of one- or twolevel symptomatic disc degeneration with posterior or posterolateral annular tears as determined by provocative computed tomography (CT) discography.87 Of the 57 patients, 38 had IDET and 19 had sham IDET. The IDET catheter was positioned to cover at least 75% of the annular tear as defined by the CT discography. Follow-up was for 6 months. This study demonstrated no significant benefit over a 6-month posttreatment period for IDET. Interestingly, neither the sham nor the treatment group made any improvement over this period; there was no placebo effect. Prospective Cohort Study on IDET Bogduk and Karasek performed a prospective cohort study with 2-year follow-up in a group of 53 patients with similar pain scores evaluating the use of IDET after establishing the diagnosis of IDD according to ISIS protocol and then performing IDET on 36 patients and comparing them to another group of 17 patients who were refused treatment by the insurers.40 The comparison group can be considered representative of the natural history of LBP treated by conventional and conservative treatment regimens, although there may be a degree of negative effect relating to the intransigence of the insurers; perhaps this group then reflects the normal situation in real medicine because the insurers often are a significant barrier to patient management. This study found that the comparison group stayed the same in regard to pain over the 2 years, with only one individual reporting partial improvement, the rest no significant improvement, and none being completely relieved at either 12 or 24 months. This contrasted substantially with those treated with IDET; at 24 months, 54% of these patients had achieved at least 50% relief of their pain, were no longer using opioids, and were at work. Even more significantly, seven patients (20%) were totally free of pain and at work at 24 months. Thus, this data meant that for IDET, the number needed to NNT for a complete resolution of pain was five, and the NNT for 50% reduction in pain was three. Furthermore, 54% of IDET patients experienced a 50% or better

Intradiscal and Peridiscal Therapies for Discogenic and Radicular Pain  465

reduction in pain and return to work and no need for opioids compared to 10% of the group undergoing typical treatment including rehabilitation.23

Efficacy of Percutaneous Intradiscal Radiofrequency Thermocoagulation (PIRFT) PIRFT has been directed into the NP and the AF; when directed into the AF it has been called RF annuloplasty (RFA). Efficacy of Intranuclear PIRFT In intranuclear PIRFT, a needle is inserted into the disc through which an electrode or flexible catheter is placed into the center of the NP of the nucleus and is slowly heated to 50 to 80° C for 90 to 360 seconds. The initial pilot study by Van Kleef and colleagues reported some success in a case series study of 39 consecutive patients with a minimum of 12 months LBP undergoing PIRFT with a 90-second 70° C lesion protocol. At 8 weeks 21/39 patients (54%), 7 of whom had had previous operation and 14 who had no operation, reported an adequate reduction in pain; at 16 months 16/39 patients (41%) reported reduction in pain.88 Barendse and coworkers performed an RCT on a cohort of NSLBP patients (n = 28) selected on the basis of positive (more than 50% relief ) AD performed at L4-5 and L5-S1.89 Patients were randomized and after the RF probe was inserted underwent PIRFT with 90 second 70° C lesions (n = 11) or sham (n = 13). At followup there was no difference between the two groups. Either the selection process was inadequate (AD alone at two levels does not comply with the diagnostic protocol for IDD) and/or the treatment method itself was inadequate. Ercelen and associates sought to determine whether the selection method or technique parameters made any difference to the RCT outcome.90 After 60 patients were diagnosed with IDD with PD, 39 patients were randomized into lesions over 120 seconds and 360 seconds both at 80° C. There was no difference between the groups at any time in the 6 months of evaluation. Pain scores were similar at 6 months to inception; the only difference was a significant decrease in pain in the first month seen in both groups. It could be concluded that PIRFT has no utility in the management of IDD or NSLBP diagnosed on the grounds of 50% relief with analgesic discography. Azulay and coworkers used a different system to perform intranuclear RF thermal lesions on 17 patients with persistent IDD, based on at least one level positive PD, for at least 6 months (mean duration was 50.6 months).91 The criteria for diagnosing DP was abnormal T2-weighted images and if no radicular pain was present, disc bulging, or herniation. Treatment was not performed if the disc height was more than 50% reduced. The technique was different from previous descriptions; 0.9% saline solution was injected into the NP, impedance levels were monitored, and each disc took about 40 minutes to treat. It was considered that this treatment should deliver safe, persistent, comprehensive heat to the AF at a sufficient degree to cause neural ablation. Using 50% pain relief as a marker of success, 15 patients were responders at 1 month (88%), 9 at 3 months (53%), and 12 at 6 months (70.6%). Efficacy of Annular PIRFT (Radiofrequency Annuloplasty with discTRODE) There is one RCT study on RFA. As with intranuclear PIRFT, the RCT showed no benefit over placebo treatment.92 RFA has also been compared to IDET in trial with 42 patients matched into each

treatment, with follow-up at 2 weeks and then at 2, 3, 6, 9, and 12 months; the IDET group had significantly better results from the 3-month period.62 In the IDET group VAS decreased from 7.4 ± 1.9 before IDET to 1.4 ±1.9 at 1 year follow-up, compared to a change from 6.6 ± 2.0 before to 4.4 ± 2.4 at 1 year after RFA. Finch93 performed a case-controlled series on 46 patients with at least 6 months of LBP diagnosed as IDD at a single level. Thirtyone patients underwent RFA and the remaining group who could not get funding for the procedure persisted with usual care. After 12 months, the VAS decreased significantly by 37% in the RFA group, and did not change in the other group. Disability, as measured by the Oswestry Disability Index (ODI) also improved. Subsequently, Kvarstein performed an RCT using RFA or sham RFA with the discTRODE probe with 10 patients in each group and followed the patients at 6 and 12 months.92 After selection according to strict criteria including positive PD with concordant pain at more than 7/10, patients underwent heating following the 10-minute protocol established by Finch,94 which is incremental heating starting at 50° C increasing by 5° C every second minute ending with a 4-minute interval at 65° C. There was no difference between the groups.

Efficacy of Disc Biacuplasty Disc biacuplasty is in its infancy. Its safety has been studied by Kapural and colleagues,95 who found that it provided a more generalized heat throughout the posterior AF than did IDET, while not heating the CNS to excess. After a reporting successful outcomes on two patients,96 one of whom had previously had a surgical discectomy,97 Kapural and coworkers reported on a 6-month pilot trial on 15 patients with IDD diagnosed on PD—all with disc heights of more than 50% of controls.98 Reassessment occurred at 6 and 12 months.98,99 At 6 months, 13 patients were reassessed. The median VAS had reduced from 7 (±1) to 4 (±1) at 1 month, and stayed much the same at the 6-month and 12-month assessments. Disability and physical function scores also improved but the differences were insignificant. Opioid use continued to decrease after the 6-month follow-up.

Comments on Pulsed RF Most studies on RF treatment use constant current RF (300 to 500 kHz) electric current energy to heat tissue adjacent to the active needle tip. In contrast, pulsed RF (PRF) treatment uses brief pulses of RF (~300 kHz) electrical current to induce similar voltage fluctuations at the treatment site without the thermal heights that cause tissue coagulation. Because the “lesions” are low temperature, they do not cause side-effects, such as post-RF neuropathic pain. However, it could also be argued that these low temperature lesions have limited ability to do much when the RF pulses have been turned off. Pulsed RF does not cause neural damage. A study on rat sciatic nerve compared the results of PRF lesions to that of RF lesions at 42° C and 70° C for 120 seconds. When the sciatic nerve was studied histologically at 21 days, it was recorded that most axonal damage occurred with the RF 70° C group.100 PRF does not cause significant damage to neural tissue,100 and any changes seem to be reversible.101 In egg white, PRF starts to produce minimal thermocoagulation at 60° C; above this temperature, PRF produces coagulation similar to, but smaller than, that of RF at the same temperature.102

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466  Spine

Gray communicant block

Sinovertebral nerve block

Gray ramus communicans

Sinovertebral nerve L5

L5

L4 spinal nerve dorsal root ganglion

PRF has been compared to RF treatment in the management of ZJ pain and been found to be substantially inferior. When 2 Hz PRF was compared to RF denervation at 80° C and to injection of local anesthetic for the treatment ZJ pain, with needles placed adjacent to the relevant medial branches or dorsal rami, there was a decrease in the VAS and disability scores at 6 and 12 months in the RF group but not the other two groups: PRF had a better short term outcome than did the control group but the improvement was not maintained at 6 or 12 months.103 Various studies have pilot-tested PRF. Intradiscal PRF has been pilot tested in a group of patients with IDD. It is theorized that high-voltage, long-duration intradiscal pulsed radiofrequency with the electrode in the center of the NP might work not from thermal effects but by exposure to electric fields.104 One pilot used PRF for 20 minutes at a setting of 2 × 20 ms/sec and 60 V on eight patients: it reported a reduction of pain score of 4/10 at 3 months and seven of eight patients were pain free at an average follow-up of 12.8 months.104 Pulsed RF has never been tested by an RCT and it seems that these results can be suitably ignored until an RCT on the efficacy is reported for any pain situation and then for the management for the management of DP or IDD.105

Neural RF Thermocoagulation for Discogenic Pain Conceptually, the possible minimally invasive targets for the treatment of a painful disc include the collagen and neural tissue within the disc, as well as the direct nerve supply of the disc (the sinuvertebral nerves, and the gray rami communicantes). As discussed earlier, it is difficult and perhaps impossible to selectively block the sinuvertebral nerve. The rami communicantes nerves are more accessible. However, both nerves innervate tissue other than the disc, so selective denervation of the disc is probably not possible in any case (Fig. 40-4).

Figure 40-4  Innervation of the lumbar disc. Diagnostic and therapeutic injections, and thermal lesions, can target the sinuvertebral nerves and gray rami communicantes.

Gray Rami communicantes The efficacy of treatment to these nerves has not been established at any stage. Although RF of the gray rami communicantes was described in 1988 as being well tolerated and at times seemingly successful, it was noted that there was a discrepancy between clinical outcomes and the information gleaned by diagnostic blocks.106 Simopoulos and coworkers used L2 ramus communicans blocks as a basis for performing L2 ramus communicans RF lesions at 80° C for 60 seconds, and in a pilot study of five patients reported “consistent pain relief after a minimum of two radiofrequency lesioning treatments approximately 4 months apart.”107 However, there has been an RCT of RF treatment of these nerves that has established possible efficacy. Oh and Shim performed an RCT on a group of patients who had been diagnosed with IDD according to strict protocol and subsequently had failed treatment with IDET.108 Patients were then excluded if they had subsequent positive medial branch blocks for ZJ pain, and were included after they reported a 50% or greater improvement in pain following a diagnostic block of the appropriate ramus communicans with 2 mL 2% lidocaine and 1 mL contrast medium. The treatment group (n = 26) received RF thermocoagulation (Stryker system) of the ramus communicans nerve at 65° Cfor 60 seconds as well as local steroid injection; the control group (n = 23) received an injection of lidocaine without RF. Patients were followed only for an average of 4 months, and VAS scores were significantly lower in the treatment group at that time. In the treatment group VAS changed from 7.1 to 3.8 (± 1.1) and SF 36 subscales for bodily pain and physical functioning also improved significantly. There was no statistical change in the control group. This is an interesting study that needs to be replicated. These nerves have also been injected in patients with refractory pain in association with osteoporotic vertebral compression fracture. In one retrospective study, gray rami communicantes blocks with local anesthetic and steroid at the fracture level produced or coincided with a modest improvement of pain over a

Intradiscal and Peridiscal Therapies for Discogenic and Radicular Pain  467

9-month period, with decreased analgesic requirements in 42% and medium-to-high patient satisfaction in 75%.109

Sinuvertebral Nerve Treatments There is some reported evidence that the L2 nerve root might innervate the lower lumbar discs. If so, it might be possible to perform RF lesions to these nerves. However, it should be noted at the outset that bilateral L1 and L2 dorsal root ganglion (DRG) blocks with injectate including 4 mL bupivacaine 0.5% did not give any pain relief in 12 patients with IDD diagnosed with PD.110 As noted earlier, these nerves supply structures other than the disc, and any efficacy from sinuvertebral nerve treatment might have nothing to do with DP. Murata and associates performed an RCT of L2 nerve root block on patients with NSLBP and/or radicular pain, reporting that the treatment group who had L2 spinal nerve root block with 1% lidocaine and 3.3 mg dexamethasone had a reduction of pain from 69/100 to 14/100 at 5 minutes and the control block group with the same medication at a depth of 2.5 cm had insignificant pain reduction from 68/100 before the injection to 62/100 5 minutes later; incidentally, they also reported a modest treatment effect at 1 and 10 weeks postinjection.111 They found that almost all patients with LBP or radicular pain had significant reduction of pain following the L2 nerve root injection, although it was not clear whether the leg pain was true radicular pain. Another study on the L2 nerve root was that of Nakamura and colleagues, who injected the L2 nerve root in 33 patients with NSLBP, some of whom had sciatica, and reported that needle insertion produced pain radiating to the low back in 23/33 injections, that LBP decreased substantially or totally, and that sciatica was not changed at all in the nine patients with sciatica.112 Furthermore, as sensory nerves from the L2 and L5 vertebral bodies may enter the paravertebral sympathetic trunks and reach the L2 DRG, Ohtori and colleagues performed an RCT on patients with LBP after acute L3 or L4 osteoporotic lumbar vertebral fracture. The treatment group had an L2 spinal nerve root block with 1.5 mL 1% lidocaine and the control group had a subcutaneous injection. Both groups had pain relief that was greater in the treatment group at 1 hour, 1 week, and 2 weeks after treatment, but there was no relief after this time in either group. It was concluded that the L2 DRG might innervate the L3 and L4 vertebral bodies in humans.113 In fact, this study randomized these patients into a treatment and a control group. The treatment group had injection of 1.5 mL 1% lidocaine directed onto the L2 nerve root with fluoroscopic control with contrast and the control group had the same injectate given subcutaneously. In the treatment group, VAS preblock was 70 ± 25 and VAS at 1 hour was 35 ± 23; in the control group, VAS preblock was 72 ± 22, and VAS at 1 hour was 56 ± 23. That is, although there was a possible trend for those patients with nerve root injection to have a decrease in pain, the confidence limits overlapped. It was not clear if any patient had 100% reduction in pain, a figure that might attract more interest if the L3 and L4 vertebral bodies are substantially innervated by the L2 DRG. Furthermore, Mendez and coworkers assessed the ability of anesthetic infiltration of the L2 spinal nerve to predict the results of PD. In 40 cases, L2 spinal nerve blocks were performed at least 2 weeks before PD. It was found that L2 nerve root block predicted the PD outcome in 46.5% of cases only, and the likelihood ratio of close to 1.0 determined that L2 nerve root block is not a surrogate for PD.114

Even if sinuvertebral nerve blocks eradicated pain and it was decided to treat with RF, the proximity of the sinuvertebral nerve to other structures—not the least being the spinal nerve root—makes such heating untenable. Sluijter has proposed the use of pulsed RF (PRF) as a nondestructive method of exposing tissue to RF electric fields.115 However, there is limited evidence that supports the use of low temperature lesions in any area of pain medicine. In a case series report, Tsou and associates performed PRF on the L2 DRG for patients with NSLBP without leg pain and added L3-S1 DRG for those with leg pain. The greatest improvement in pain occurred at 3 months, and at 3 and 12 months approximately 45% of patients had pain relief of 50% or more.116

Intradiscal Chemical Therapies for Discogenic Pain Proliferants In one study, 30 patients with chronic NSLBP for an average duration of 8.5 years were diagnosed with IDD on PD and treated with an intradiscal injection of a solution containing glucosamine and chondroitin sulfate combined with hypertonic dextrose and dimethyl sulfoxide (DMSO), which is an industrial solvent also used to treat interstitial cystitis. At an average posttreatment time of 12 months, Roland-Morris scores were 6.4±1.0 from 12.0±0.9 and VAS 3.0±0.4 from 6.1±. Overall, 17/30 (57%) did very well with average of 72% of disability scores and 76% of VAS, whereas the other 13/30 (43%) showed little or no improvement.117 The effect of intradiscal injection of a solution consisting of 1.5 mL 50% dextrose in water and 1.5 mL 0.25% bupivacaine was measured on patients with moderate-to-severe DD without herniation and with positive PD. Patients underwent biweekly injections (average number 3.5). At 18 months, 43% of patients had sustained improvement with an average reduction in VAS of 71%.118 In a pilot study, Derby and colleagues tested intradiscal injection of glucosamine and chondroitin sulfate combined with hypertonic dextrose and DMSO (N = 35) against IDET (N = 74) in patients with IDD diagnosed with PD.119 At 6 to 18 months the VAS improvement was 2.2 for the injection group and 1.3 for the IDET group, with 66% of the injection group and 47% of the IDET reporting feeling better.

Steroids Intradiscal steroids have been reported for the treatment of disc problems including putative DP.120-125 They have been shown to be no more effective than placebo at 2 weeks and 1 year in patients with a positive PD.120,121 They might be effective in the short term for some patients with vertebral end-plate changes. The rationale for their use is that they interrupt the inflammatory pathway in their action as a phospholipase A2 inhibitor. The first reports were by Feffer, who subsequently reported on 244 patients injected with intradiscal steroids finding that at ­follow-up between 4 and 10 years, 47% had recovered and the patients with predominantly LBP were more likely to recover.123,124 Graham compared chemonucleolysis with chymopapain to intradiscal hydrocortisone, with 20 patients in each group, in a double-blind study of patients with “discogenic back pain and sciatica.”126 The 2-year post-injection survey by an independent observer revealed that there was no statistical significance between the

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results, although the trend suggested superiority of CN, which had nine good, three fair, and eight unimproved results in 20 patients, contrasting with hydrocortisone, which produced three good, eight fair, and eight unimproved results in 20 patients—one patient dying from unrelated causes. Then Wilkinson and Schuman performed 42 intradiscal injections on a series of 29 patients with NSLBP, and 18 injections on 13 patients with NSNP, none of whom had classic symptoms or signs of true radicular pain, although some were reported as likely to have radicular pain.127 All of the patients underwent analgesic and/or contrast discography, which was reported as showing morphologic changes consistent with degeneration in 27 of the 29 patients: pain provocation was not reported on. Each disc was injected with between 40 mg and 80 mg suspension of methyl prednisolone. There was a fair degree of pain relief early on, and a few patients had relief lasting 6 months to several years. No conclusions could be necessarily drawn from this, except that these injections prevented only 11 of the 29 of the lumbar group from having surgery, and most of these did poorly with surgery anyway. Simmons reported on patients who had positive PD at 2 weeks, finding that there was no difference between those injected with steroid and those injected with bupivacaine.121 Khot reported on a similar cohort of 120 patients and found no difference at 1 year between injection of saline and steroid.120 However, Fayad investigated steroids in patients with NSLBP who had not recovered with 3 months of conservative treatment.122 This early intervention was found to be more successful at 1 month in those who had Modic type 1 changes or Modic type 2 changes with predominantly edematous changes. At 3 months, the outcomes were similar in all patients with any Modic type 1 or 2 changes.

Methylene Blue Methylene blue (MB) is attracting increasing interest in the management of IDD. It was first reported as having a possible role in medicine in 1885 by Erlich and by 1928, it had attracted significant interest from its use as an indicator to its possible role as a therapeutic agent.128 Its neurotropic actions and its nerve blocking or neurolytic action129,130 have been used for a variety of applications.131 MB has been used, for example, in the treatment of methemoglobinemia, cyanide poisoning, carbon monoxide poisoning, pruritus ani, and Alzheimer disease. Sheng and coworkers introduced it as a possible treatment for pain by successfully injecting MB with procaine into pelvic fracture sites for the management of fracture pain, with each injection giving pain relief for about 3 weeks.132 MB, by inhibiting the enzyme guanylate cyclase, blocks the accumulation of cyclic guanosine monophosphate (cGMP), thereby reducing the responsiveness of vessels to cGMP-dependent vasodilators like nitric oxide. Nitric oxide is a final common mediator of cartilage degradation.133 As a consequence, it has been tested as a potential intradiscal treatment for DP. In a novel study, Peng and associates injected patients who were otherwise scheduled for lumbar interbody fusion for back pain with an intradiscal injection of one mL of 1% MB followed by 1 mL of 2% lignocaine.131 The criterion for selection was failure of other nonsurgical treatment for at least 6 months, and finding a painful abnormally morphologic disc on PD (no comment was made about adjacent controls). At a mean follow-up period of 18.2 months, 87% (21/24) reported a total or substantial relief of low back pain and improvement in

physical function. VAS pain scores pretreatment, and at 3, 6, and more than 12 months were 7.52±1.31, 2.50±2.09, 2.37±2.06, and 2.18±1.79. Oswestry disability scores (ODI) over the same period were 48.71±5.28, 17.42±14.76, 16.79±15.02, and 15.38±13.63. That is, VAS and ODI dropped significantly early on and the improvement was maintained. Peng and coworkers then ran an RCT on MB treatment for minimum 6 months” DP, with 36 patients in each group. At the 24-month follow-up, both the groups differed substantially with respect to the primary outcomes. The patients in MB injection group showed a mean reduction in pain measured by NRS of 52.50, a mean reduction in Oswestry disability scores of 35.58, and satisfaction rates of 91.6%, compared with 6.91, 1.68, and 14.3%, respectively, in placebo treatment group. Regular medication was still used by 42.9% of the placebo group 24 months after randomization, but in only 8.3% of the MB injection group. No adverse effects or complications were found in the group of patients treated with intradiscal MB injection. Thus, MB appears to be a safe, effective, and minimally invasive method for the treatment of IDD.4 As Peng and coworkers pointed out,4 these outcomes are similar to those reported for fusion or artificial disc replacement,134,140 and MB treatment has a significant advantage of now having been tested with a RCDBT.

Regenerative Therapies for Discogenic Pain Disc homeostasis is mediated by various substances including cytokines, growth factors, enzymes, and enzyme inhibitors. Proteoglycans play a central role in the function of the disc, and restoration of normal proteoglycan production is a key component of minimizing DD.141 Whether this translates to less LBP is unknown, however. Proteoglycan production can be elevated by up-regulating their production or down-regulating proinflammatory cytokine-mediated catabolism.142 The cytokine TNF-α is found in increased quantities in DD and contributes to matrix degradation by increasing MMP-2 (also called gelatinase) activity.143 Gelatinase cleaves the fragments of collagen that have been degraded by collagenase (MMP-1), which itself has a more direct action as it cleaves type II collagen.144 TNF-α also has a possible role in DP through its role in neuronogenesis.145 Etanercept, a TNF-α blocker, has been injected intra­ discally in a double-blind, placebo-controlled pilot study and found to be a safe but ineffective treatment for chronic radicular pain and IDD.146 Biologic substances and drugs can be delivered to the disc directly and also via gene therapy using a gene vector.141 Intradiscal delivery is favored over intravenous delivery because IV solutes do not penetrate the central disc and concentrations dissipate rapidly.147 However, because it is likely that molecules required to affect homeostasis will require a sustained interface, genes encoding the recombinant or natural proteins may turn out to be the optimal method of delivery.148 An example of a regenerative agent under study is osteogenic protein (OP-1). It is from the bone morphogenetic protein (BMP) family, and is unique in that it is both proanabolic and anticatabolic.149 OP-1 is safe when injected into rat NP and epidural space.150 In experimental studies, growth differentiation factor 5 (GDF-5) and osteogenic protein 1 (OP-1) stimulate proteoglycan and collagen synthesis in the disc, with corresponding in vivo reversal of DD features including restoration of disc height,

Intradiscal and Peridiscal Therapies for Discogenic and Radicular Pain  469

improvement in MRI scores, and histologic grading.151,152 It has therefore been proposed that OP-1 can be used in combination with chemonucleolytic agents such as collagenase to prevent the inevitable degeneration related to chemonucleolysis. In rabbit models, the combined use reversed the decrease seen in disc height of those injected with collagenase alone.153 Perhaps it could also be used in combination with intradiscal thermal therapies, as they, as noted earlier, have been shown to stymie tissue regeneration. However, it may be that the effect of these agents may be insufficient to alter the molecular structure of the disc to a significant extent to ameliorate pain. Stem cell therapies have also been investigated. It appears that, at least in rabbits, mesenchymal stem cells transplanted into disc tissue survive for many weeks and have the potential to promote disc healing.154 However, when 10 patients with a positive PD underwent intradiscal injection with hematopoietic precursor stem cells (HSCs) and a subsequent 2-week course of hyperbaric oxygen therapy and followed up at 6- and 12- month intervals there was no improvement.155 Although there are abundant animal experimental studies demonstrating the potential for growth factor and other related restorative therapies, there are few studies that can be translated to humans. Even if disc homeostasis can be positively affected, this does not necessarily mean that LBP will be cured.

Intradiscal Chemical Therapies for Radicular Pain Chemonucleolysis, Chymopapain, Collagenase, Chondroitinase, and Ethanol After chymopapain (CP) was injected into the NP for the treatment of sciatica in 1963 in a process coined chemonucleolysis (CNL),156 various high-quality studies determined that it was a preeminent treatment for radicular pain because of disc prolapse. It was used in the United States for about 20 years until its demise, which was caused by a variety of political factors causing less utilization and withdrawal by its manufacturers.157 Subsequent to CP, other materials, such as collagenase,158 ethanol,159 and chondroitinase have been developed as potential surrogates.160 CP was definitively proved to be an effective and safe treatment for the treatment of radicular pain owing to disc prolapse but not disc sequestration.161 Its withdrawal indeed defies logic. Even though microsurgery for this condition is relatively safe and effective, it may be that these chemical therapies or other surrogates will be developed. Collagenase certainly showed promise. Ethanol has also been shown to be effective,159 but is difficult to handle. Subsequently, radiopaque gelified ethanol (RGE) has been developed and assessed.162,163 In cervical disc prolapse, the results were rated as satisfactory in 89.5% of patients with no adverse events recorded during the procedure or after.163 In another trial, 276 consecutive patients were divided into two groups, the first containing patients with simple disc prolapse and the second those with disc prolapse in association with more severe symptoms, disc sequestration, or foraminal/canal narrowing. The first group (A) was treated with RGE and intraarticular steroids only. The second group (B) was subdivided into two, the first being treated with RGE and automated percutaneous discectomy, and the third (C) with RGE and radiofrequency nucleoplasty. At follow-up, very good or good results were obtained in

202/221 (91%) patients in group A, in 37/44 (84%) in group B, and in 9/11 (82%) of group C. There was no allergic complication in any of our patients.164 Any chemical therapy should aim to be as effective as CP was. After various studies had shown good results and the optimal dosage,165,166 a high-quality and extensive study on CP for the treatment of disc prolapse was performed by Gogan and Fraser that proved CP was significantly superior to placebo.167 They compared 30 patients injected with CP with 30 patients injected with saline. At 10 years, 80% of the CP patients, who were still blinded to the original treatment, regarded the injection to be successful, compared with 34% for the saline group (P =.0006). Laminectomy had been required in 20% of the CP patients, compared with 47% of the saline patients (P = .028). Seventy-seven percent of the CP group was assessed by a blinded independent observer to be at least moderately improved, compared with 38% for the saline group (P = .004). Over these 10 years, the results for benefit of CP over placebo were maintained: for example, at 6 weeks posttreatment, 73% of CP patients and 37% of placebo patients were considered to have a successful outcome; at 6 months success was 80% and 57%;168 at 2 years, 77% and 47% and at that 2-year review 57% treated with CP were free of pain, compared to 23% in the saline group.169 A systematic review/meta-analysis of 22 eligible trials concerning CP found that chemonucleolysis with CP was superior to placebo and was as effective as collagenase in the treatment of lumbar disc prolapse, with a summary risk ratio estimate for pain relief as outcome of 1.51 (95% CI: 1.27 to 1.80) for the comparison between chemonucleolysis versus placebo, and 1.07 (95% CI: 0.95 to 1.20) for the comparison between chymopapain and collagenase.170 In a 5-year clinical follow-up assessment of a prospective DBRCT of chemonucleolysis using CP or collagenase for the treatment of 6 weeks or more radicular pain caused by disc prolapse short of extrusion revealed good and excellent results in 72% of the CP group and 52% of the collagenase group when progression to surgery was considered a failure. After injection, 18% of the CP group and 28% of the collagenase group underwent microdiscectomy at the injected level. Of the reexamined patients who did not have microdiscectomy, 100% of the CP group and 93% of the collagenase group had good and excellent results. Thus, in the doses used, CP (4000 IU) and collagenase (400 ABC units), collagenase was still effective but not as effective as CP. Both were considered to be safe when injected under controlled conditions.171 However, a review of all treatments on disc prolapse indicates that overall discectomy produces the best results. Gibson and Waddell analyzed all randomized controlled trials published up to January 1, 2007 on the treatment of disc prolapse, reporting that discectomy produced better clinical outcomes than chemonucleolysis, which itself was better than placebo.172 As an example, Van Alphen and colleagues performed a randomized trial comparing open discectomy with chemonucleolysis in 151 patients suffering from a disc herniation at L4-5 or L5-S1. In the immediate postoperative period there was an increase in radicular pain in 16 patients (22%) in the chemonucleolysis group compared to none in the discectomy group.173 Within a follow-up period of 1 year, 18 patients (25%) required open discectomy following failed chemonucleolysis; two patients (3%) in the discectomy group needed a second operation. Open discectomy following previous chemonucleolysis was successful in only 44% of cases. Comparison of the final results of the two modes of treatment 12 months after the last

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intervention (including second treatment) did not reveal any significant differences.

Ozone Ozone, injected as an ozone/oxygen mixture, is considered to have a redox action on NP proteoglycan,174 and possibly an antiinflammatory action. A meta-analysis of the use of ozone for the treatment of disc prolapse presented at the Society of Interventional Radiology meeting in 2009 by Murphy, who disclosed a financial interest in the manufacturing of the device used, reported that there were 24 related articles of which 13 (with 8000 patients) met inclusion criteria.174 There was a 79.9% reported improvement in the Modified MacNab scale with this treatment. However, there is virtually no reasonable data on which to reach a conclusion that this treatment has significant benefit. Most reports relate to the treatment of radicular pain for disc prolapse.174-178 One literature review found five controlled studies, all considered to have methodologic limitations, supporting the efficacy of ozone over microdiscectomy.179 However, a controlled trial by Wu and coworkers in which two groups of 108 patients presenting with lumbar disc prolapse were treated using surgery or the injection of oxygen-ozone combined with collagenase into the lumbar disc or the epidural space. The difference in the success rates of 86.11% and 88.89% in the minimally invasive group at 3 and 12 months, respectively, and 92.59% and 95.37% in surgical group were not statistically significant.178 There have also been reports of possible serious side-effects from this therapy.180,181

Saline Intradiscal saline, which when injected under high pressure ruptures the thinned posterior longitudinal ligament, has been used and studied for the management of disc prolapse. Tearing of the ligament is confirmed by a sudden loss of resistance to injection and leakage of contrast medium from the disc to the epidural space. It was reported to be successful in patients with large disc herniations.182 However, there is insufficient data on its use to draw any conclusion.

Percutaneous Disc Decompression for Radicular Pain Nucleoplasty Nucleoplasty, the process of disc decompression patented by ArthroCare, uses RF energy to ablate soft tissue and thermal energy to coagulate soft tissue radiofrequency energy (Coblation (ArthroCare, Sunnyvale, CA)). The catheter (Perc-D Coblation Channeling Wand) is inserted into the disc under fluoroscopic control. As the catheter is advanced to the required depth, it makes a channel as it ablates surrounding tissue. Then, as it is withdrawn, the thermal lesion coagulates adjacent tissue. About six channels are created in this way in a process named by the manufacturer as “coblation.” Nucleoplasty is also known as percutaneous radiofrequency thermomodulation or percutaneous plasma discectomy. Nucleoplasty is primarily used for the treatment of radicular pain secondary to contained disc protrusion. It is of no use for extruded or sequestrated discs. It has also been proposed secondarily as a treatment for DP or IDD. However, from a theoretical

perspective, this effect is unlikely if the mechanism is reduction in NP pressure. The degenerate NP has already lost pressure, and further destruction would be likely to increase the loads on the AF, thereby increasing the likelihood of DP. Gerszten anc colleagues performed a prospective audit of 67 patients (mean age 41 years) with primarily radicular pain owing to a contained disc herniation who underwent nucleoplasty with the Perc-DLE SpineWand and, although they reported improvements in disability at 3 and 6 months, the mean improvement of VAS at 3 months was only 1.3/10.183 A systematic review of the literature relating to mechanical lumbar disc decompression with nucleoplasty reported that there is level II to III evidence for mechanical lumbar percutaneous disc decompression with nucleoplasty in treatment of leg pain, but no evidence available in managing axial low back pain.184 Cervical spine nucleoplasty is at a very early stage of development and research. Percutaneous nucleoplasty and percutaneous cervical discectomy seem to be low-risk procedures that both lead to about 80% significant clinical improvement for the treatment of contained cervical disc herniation.185-187 It should be noted, however, that when cervical discectomy, physiotherapy, and no management was compared at 12 months in the management of cervical radicular pain owing to disc prolapse, the outcomes were identical.188 Bhagia and coworkers studied the complications and side effects of nuceloplasty in a prospective study in 53 patients; they found at 24 hours needle point entry soreness (76%), new numbness and tingling (26%), increased intensity of preprocedure back pain (15%), and new areas of back pain (15%). At 2 weeks, no patient had soreness at the needle insertion site or new areas of back pain; however, new numbness and tingling was present in 15% of patients and two patients (4%) had increased intensity of preprocedure back pain.189 However, there were statistically significant reductions in back and leg pain.

Laser Lasers have been used in medicine since the 1960s. Percutaneous laser disc decompression has been used as a treatment for radicular pain secondary to contained disc herniation. A systematic review of the literature found only Level II-2 evidence for this use.190 However, laser has also been studied for the treatment of IDD. Percutaneous endoscopic laser annuloplasty (PELA) targets the AF alone. It uses a small endoscope enabling the use of Ho:YAG laser, irrigation and light. This tool used with an extreme posterolateral approach into the posterior AF allows entry into the disc with minimal damage. It was studied in 30 patients with chronic disabling back pain of at least 2 years over a 10-month follow-up period who also had (1) DD and a HIZ on MRI and (2) positive PD at only one level. The discography had been performed just prior to the procedure, and thus the cannula could be placed very close to any annular tear. The mean VAS score improved from 8.0 to 2.4 and the modified Macnab’s criteria also showed a good outcome, with a success rate of 90.0%.191 PELA needs to be studied further.

Automated Percutaneous Lumbar Discectomy Automated percutaneous lumbar discectomy (APLD) is performed with a pneumatically driven, section-cutting probe that removes disc material about 1 cm anterior to the herniation. There have been two RCTs comparing chemonucleolysis (CN) favorably to

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APLD.192,193 However, two RCTs compared APLD with microdiscectomy.194,195 In the Chatterjee study, 71 patients with contained disc herniations and radicular pain were treated with either procedure and satisfactory results were seen in 80% of the microdiscectomy group and only 29% of the ALPD group.194 In the other study, only 27 patients were ultimately followed up from 5735 screened patients, of whom 95 were found to be eligible and 36 were enrolled; the success rate in each group was 40%.196

Technical Performance of Intradiscal Procedures Disc Access As in any medical intervention, spinal procedures should be performed by a practitioner who understands the reasonable indications for the procedure, can perform the procedure with a high degree of technical skill, can look after the patient and manage immediate and subsequent complications, and can manage those who fail to respond to that particular form of treatment. The procedures should be performed in an operating room using optimal sterile procedure with contemporary anesthetic equipment. An operating room has the advantage of trained theatre and recovery staff. Many procedures are made substantially easier for the patient when performed using some form of sedation, but sedation can have its down sides. Sedated patients are unable to inform the operator about pain, and the risk of inadvertent nerve root injury may be increased. The adequate use of local anesthetic infiltration can be just as effective. Most procedures can be performed as day procedures. The operating table should be one that is of a suitably thin dimension to allow C-arm fluoroscopic access, has no metal or other material that obscures fluoroscopic views, and can be simply moved up and down, caudad and cephalad, and obliquely. The C-arm fluoroscope should be easily mobile both around the patient and the operating room.

Position of Patient When the patient has arrived in the theatre he or she is positioned on the table. The position chosen will depend on issues of stability, (the best position is one where the patient will not be able to move), operator preference, and access. Once a particular position is chosen, ensure that the position is solid with the use of plastic wedges, pillows, towels, and the like. In the lumbar spine, it is best to minimize the lumbar lordosis, particularly when the target disc is L5-S1. Various positions are described: typically prone, oblique (modified Sim’s), and lateral.

Identify the Anatomy and Mark the Entry Point The next most important preparatory concern is the correct identification of the spinal vertebral levels. It is essential to have documented the intended target disc and vertebral levels; this requires review of past investigations such as discogram films, MRI, CT scan, and plain radiographs. Extra care is essential where there are lumbosacral anomalies especially sacralization. The differentiation of T12 and L1 can be difficult where the twelfth rib is small or vestigial. It is best, once the plan has been made to bring the C-arm into play, to mark the target vertebral levels with a marking

pen and to mark the intended site of needle entry. Variability in C-arm rotational movement capabilities sometimes prevents a good oblique view from being obtained; in such an instance the patient may need to be propped into a more oblique position with the use of a foam wedge or a towel. It is also advisable to swing the C-arm into the lateral view to ensure that there is no impediment, such as an arm board, to full access. It is useful for the radiographer to record the angles used to find key target points so that the C-arm can be returned to the same alignment after prepping.

Prepare the Needle Despite the risk of infection being low, most practitioners do not allow the gloved hand to touch the distal end of the needle or device that will be entering the disc. Sometimes it is necessary to add bends or curves to needles or devices. If this is the case, interpose sterile gauze between the gloved hand and the needle and curve a larger introducing needle while it is still within its plastic sheath. Needle manipulation with the use of the fluoroscope should be second nature by the time these procedures are performed. It is essential to know the angles required to position the needle or device in the center of the disc, in the AF, or on a particular nerve. Understand where the bevel of the needle is and the effect the bevel or a curve will have on its introduction.

The Procedure The process for discogram is also described in Chapter 38. Any intradiscal procedure requiring injection into the NP is performed using this method. After intravenous access has been obtained, the patient is prepped and draped, and, if required, adequately sedated. The entry site and the proposed needle track can be injected with local anesthetic with a 3.5-inch spinal needle. Standard Entry to a Lumbar Disc The operator must be aware of the position of the needle or device tip at all times; this requires repetitive C-arm repositioning into PA, oblique, and lateral views. Due to the natural lordotic curve of the lumbar spine, the C-arm is moved in a cephalocaudad direction to achieve a direct visualization into the index disc; the vertebral body should be as close to squared off as possible. The process of getting the end plate square or crisp is commonly referred to as “crisping” the disc. The vertebral end plates above and below the disc are seen to move from an elliptoid image to a crisp line as the angulation approaches ideal view to that disc (Fig. 40-5). The C-arm is then moved in an oblique way to the side of entry. The superior articular process of the ZJ is seen to move across the disc space as the obliquity increases and ideally is positioned at the midpoint of the disc. The skin entry site for direct disc access in the lumbar spine is found as the C-arm is rotated axially from a direct PA position to an oblique position when the superior articular process of the subjacent vertebra bisects the target disc space (Fig. 40-6). The entry point is just lateral to the superior articular process at the midpoint of the crisp disc. A 14-gauge intravenous cannula is ideal to breach the skin in a down-the-beam view toward the disc. When the stylet is removed from the intravenous cannula, the needle can be placed through the cannula aiming at the disc. It is common to gently brush the lateral aspect of the superior articular pillar and, at this point, the patient may have minor discomfort. When using a curved needle, it is best to allow the natural curve to bounce off the superior articular process when there is an immediate

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Figure 40-5  Crisping the disc: the superior end plate of L5 is crisp; the ­inferior end plate of L4 is ellipsoid.

Figure 40-6  An oblique view of the L4-5 disc showing the needle aimed at the midpoint of the L4-5 disc.

sense of release or loss of resistance; then the curve is rotated 180 degrees, such that the concave side of the curve is now medial and the approach angle into the disc is improved. Lateral and PA images may then be checked under fluoroscopy prior to entering the disc. Contact with the outer AF is associated with increased pressure. Lateral and PA views are required to determine final needle position (Fig. 40-7). Clearly, for discography or other intranuclear injection, the needle is placed centrally within the NP, whereas variations on this are more ideal for nucleoplasty and IDET. The most difficult target disc is L5-S1. The iliac crest frequently gets in the way of a direct en pointe needle approach. The anatomical target is first the bony notch between the sacral ala and the superior articular facet of S1. Difficulty occurs when the iliac crest overlaps the down-the-beam insertion, or when the L5 transverse process gets in the way. These problems can be overcome by using a commercially bent needle or by putting a bend into the straight needle, and by using needle skills such as applying various torques to the needle as it is inserted. The trocar bevel should also be pointed in the intended direction of the needle.

NP and the AF. When the Crawford needle has breached the AF, PA and lateral views are required to determine this position. In the lateral view, the spine wand is then introduced through the Crawford needle. It is carefully advanced until the tip is at the end of the Crawford needle and it is then manipulated across the NP until a firm resistance is felt on the anterior AF wall. Regular fluoroscopic monitoring is required to ensure that the wand has not advanced beyond the anterior vertebral margin (Fig. 40-14). A PA view ensures that the wand lies across the central aspect of the disc (Fig. 40-15). The cable is connected between the power source and the wand and power level 2 is selected (Fig. 40-16). The small spring depth lock is slipped down the spine wand while it is still in the fully deployed position; this helps to protect the wand from being inadvertently advanced beyond this point during the procedure. The wand is withdrawn so that it is deployed just beyond the end of the Crawford needle and the coblation pedal is activated. The wand is advanced in the 12 o’clock position to the fully deployed depth. Each pass is performed using coblation for 10 to 20 seconds. This is repeated rotating the hub of the wand to 2 o’clock, 4 o’clock, 6 o’clock, 8 o’clock, and 10 o’clock. Due to the curved tip of the wand, a different path is thereby created on six occasions. The wand is then removed from the Crawford needle. Commonly, cephazolin (50 to 100 mg) is injected into the disc following the procedure. The wand and introducing Angiocath sheath are then removed and a dressing is applied.

Nucleoplasty The nucleoplasty procedure is performed using a standard approach into the lumbar disc, as described earlier (Fig. 40-8). In the example shown, the L5-S1 disc has degraded and there is a small, central contained disc prolapse established as contained by discography (Fig. 40-9). In this demonstrated procedure, the needle entry is somewhat lateral to the central point described earlier (Figs. 40-10 and 40-11). When the 14-gauge cannula is accurately placed in the line of the C-arm beam aiming at the disc, then the 17-gauge Crawford needle supplied with the nucleoplasty kit is placed through the cannula toward the disc (Figs. 40-12 and 40-13). In the nucleoplasty procedure, it is ideal to be aiming at the center of the disc, although the Crawford needle is advanced only to the junction between the

IDET The approach is similar to that described for nucleoplasty, however less obliquity is required and the superior articular process does not need to be at the midvertebral body. The introducing needle is ideally placed approximately one third of the way across the disc in the PA view, but central on the lateral view, thereby lying within the AF (Fig. 40-17).

Intradiscal and Peridiscal Therapies for Discogenic and Radicular Pain  473

40

Figure 40-7  Lateral and posteroanterior (PA) views demonstrating discography needle in the NP.

Postprocedural Management Considerable reduction in postprocedural pain and stress can be achieved through adequate preprocedural counseling. Patients should be told that pain in the recovery room is common, and that it will most likely abate over the next few hours or days. Persistent reassurance is required to minimize postprocedural apprehension. Patients are routinely told to have a quiet and mostly restful 48 hours. Intermittent ice may be applied for local soreness and simple analgesics are usually sufficient. No oral antibiotics are required. If pain becomes more of a problem, then movement can be more helpful than rest. If muscle relaxants or stronger analgesics are required, usual care needs to be taken with ambulation. A back support can help in some instances. Some patients do require stronger analgesics and perhaps muscle relaxants.

Complications Figure 40-8  Operating room ready for nucleoplasty to proceed.

The stylet is removed and the IDET Spine-cath is deployed into the disc. It is best to have the concavity of the catheter tip facing medially to facilitate navigation around the AF. Gentle constant pressure is applied to the proximal hub of the catheter as it is observed under fluoroscopy to pass across the anterior AF and then to track posteriorly to the posterolateral AF. AP and lateral views are used to check catheter position, and in particular, to check that the catheter has not inadvertently deployed through a fissure into the epidural space (Fig. 40-18). At times, the catheter may not deploy to the correct position; it can then be withdrawn into the needle and redeployed with a different catheter orientation. If such manipulation fails to achieve satisfactory positioning, the catheter should be completely withdrawn from the body and the introducer needle adjusted, usually further anteriorly or to the anterolateral quadrant on the opposite side, followed by catheter placement (Figs. 40-19 and 40-20). When the device is in position, a 17-minute heat cycle to 90° C is performed. The catheter is removed and cephazolin (50 to 100 mg) is is injected intradiscally. The needle is then removed and dressings are applied.

These can be minimized by strict adherence to preprocedural screening and operative technique. In a meta-analysis of IDET, Appleby coworkers197 found the overall incidence of complications for IDET to be 0.8%; of the 17 studies analyzed, 6 reported no complications in 240 patients,39,47,50,198-200 and 23 complications were reported in another 6 studies from procedures on 246 patients.51,201-205 Of these, most resolved, but eight went on to fusion. The complications included increased radicular pain, neuropathic sensations in legs, disc herniation at the level, L5 nerve root injury, dural puncture, discitis, anterolisthesis, increased pain in back, cauda equina lesion, referred leg pain, and headache. The neurologic complications of neuropathic leg sensations, cauda equina lesion, and L5 nerve root injury all resolved. Should Antibiotics Be Used? There is no consensus regarding the use of antibiotics in intradiscal procedures. If the risk of infection from discogram is similar to that of an intradiscal procedure, then the risk of infection is extremely small. There are no randomized or controlled trials on the efficacy of prophylactic antibiotics in discography.206 Based on animal experiments,207 the incidence of postdiscography discitis is lowered with the use of cephazolin given either intravenously or in the intradiscal suspension injection. In high concentrations, contrast medium can itself inhibit bacterial growth at least to some degree, and it does not reduce the inhibitory effect of antiobiotics.208 A follow-up of 127 consecutive

474  Spine

A

B

Figure 40-9  T2-weighted MRI views. A, Lateral view showing disc ­degradation and small posterior bulge/prolapse. B, Axial view showing the central prolapse.

Figure 40-10  Entry point for nucleoplasty at L5-S1.

Figure 40-11  PA view of the entry point for nucleoplasty at L5-S1.

Figure 40-12  The Crawford needle.

Intradiscal and Peridiscal Therapies for Discogenic and Radicular Pain  475

patients having lumbar discography with contrast containing cephazolin 1 mg per mL revealed no cases of discitis. 207 However, Willems and colleagues had no cases of discitis when they performed two-needle technique discography without preemptive antibiotics on 200 patients and followed them all for a minimum period of 3 months.209 Willems and colleagues also reviewed the literature ­concerning discitis following discography. They reported on 10 papers spanning a period of 40 years from 1962 to 1990, one of which used prophylactic antibiotics and reported no cases of discitis,207 and the other 9,210-218 which when combined with the Willems study, showed that the overall rate of discitis without prophylactic antibiotics was 0.24% of all patients (12 cases in 5091 patients) or 0.091% of all discograms (12 cases in 13, 205 discs).209 Other possible complications with any of these procedures includes wound infection, superficial abscess, epidural abscess,180 discitis,180 osteomyelitis, and septic arthritis. Can Disc Puncture Itself Cause Harm? Animal models that study DD have used stab incisions into the AF because these induce generalized DD within the entire disc.26,219 In one experiment, looking for the best way to model for DD, a 21-gauge, three-puncture technique was superior to an 18-gauge,

Figure 40-13  The Crawford needle is introduced into the cannula.

one-puncture in producing disc degeneration over a shorter period of time.219 This introduces a question about the relationship between number of penetrations versus size; it may be that a smoother technique with one introduction of a thin needle has a minimal chance of producing a detrimental effect. Two studies are worth assessing in this regard. In a long-term follow-up of patients undergoing disc puncture, Carragee followed two matched cohorts of 75 each without serious LBP “illness.”220 Each subject was assessed with MRI and one group underwent L3-4, L4-5, and L5-S1 discography examination in 1997. There were 134 needle injections with a 25-gauge needle and 21 injections with a 22-gauge needle. Between 7 and 10 years after enrollment, each subject underwent a further MRI: 50 discography subjects and 52 control subjects were reassessed. The results were as follows: (1) in all graded or measured parameters, discs that had been exposed to puncture and injection had greater progression of degenerative findings compared to control (noninjected) discs—this was represented by: progression of disc degeneration, 54 discs (35%) in the discography group compared to 21 (14%) in the control group; ] 55 new disc herniations in the discography group compared to 22 in the control group; (2) new disc herniations were disproportionately found on the side of the AF puncture; (3) the quantitative measures of disc height and disc signal also showed significantly greater loss of disc height and signal intensity in the discography disc compared to the control disc; and (4) there was no statistical differences in the progression of degeneration findings between the smaller and larger gauge needles, although there was a trend to greater degeneration in the discs punctured with the larger 22-gauge needle. There was no comment made regarding the number of penetrations made per discogram. In contrast, Freeman and colleagues performed a study on IDET in live sheep.21 As part of the study, normal discs were incised with a 19-gauge needle, and again, no comment was made about the number of disc penetrations. At 18 months, there was no alteration of disc morphology compared to controls. If true, the consequences of disc puncture in discography are germane for any intradiscal procedure. It may be that the number of needle penetrations is as important as the gauge of the penetration instrument. However, if these reported effects are generalizable, they may or may not translate into symptoms and, if they do, it would seem that by now there should have been an epidemic of symptomatic disc prolapses in subjects who had undergone discography. Such an epidemic has not been reported.

Figure 40-14  Progressive lateral fluoroscopic views as the needle is advanced.

40

476  Spine

Figure 40-15  Progressive posteroanterior (PA) fluoroscopic views as the needle is advanced.

Figure 40-16  The cable is connected.

A

Figure 40-17  IDET cannula being introduced toward the L4-5 disc. IDET, IntraDiscal ElectroThermal treatment.

B

Figure 40-18  IDET cannula coiling around inside the L4-5 disc: A, Lateral view showing IDET at the posterior margin of the disc. B, PA view. IDET, IntraDiscal ElectroThermal treatment.

Intradiscal and Peridiscal Therapies for Discogenic and Radicular Pain  477

IDET: IntraDiscal ElectroThermal Treatment

5-cm active tip

IDET: IntraDiscal ElectroThermal Treatment

5-cm active tip in circumferential fissure

Figure 40-19  Schematic representation of IDET. In this image, the IDET lesion crosses the radial tear in the axial projection but would not affect the demonstrated circumferential tear. IDET, IntraDiscal ElectroThermal Treatment.

Figure 40-20  Schematic representation of IDET. In this image, the IDET lesion again crosses the radial tear and is applied in part of the ­circumferential tear. IDET, IntraDiscal ElectroThermal Treatment.

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Intradiscal and Peridiscal Therapies for Discogenic and Radicular Pain  481 169. Fraser RD. Chymopapain for the treatment of intervertebral disc herniation. The final report of a double-blind study. Spine. 1984;9: 815-818. 170. Couto JM, Castilho EA, Menezes PR. Chemonucleolysis in lumbar disc herniation: a meta-analysis. Clinics. 2007;62:175-180. 171. Wittenberg RH, Oppel S, Rubenthaler FA, et al. Five-year results from chemonucleolysis with chymopapain or collagenase: A prospective randomized study. Spine (Phila Pa 1976). 2001;26:1835-1841. 172. Gibson JN, Waddell G. Surgical interventions for lumbar disc prolapse: updated Cochrane Review. Spine. 2007;32:1735-1747. 173. van Alphen HA, Braakman R, Bezemer PD, et al. Chemonucleolysis versus discectomy: a randomized multicenter trial. J Neurosurg. 1989;70:869-875. 174. Murphy KJ. Oxygen/ozone as effective as discectomy for herniated disc pain. Society of Interventional Radiology (SIR) 34th Annual Scientific Meeting. Abstract. 2009;37:Conference Proceeding. 175. Alexandre A, Coro L, Azuelos A, et al. Intradiscal injection of oxygenozone gas mixture for the treatment of cervical disc herniations. Acta Neurochir Suppl. 2005;92:79-82. 176. Muto M, Andreula C, Leonardi M. Treatment of herniated lumbar disc by intradiscal and intraforaminal oxygen-ozone (O2-O3) injection. J Neuroradiol. 2004;31:183-189. 177. Paradiso R, Alexandre A. The different outcomes of patients with disc herniation treated either by microdiscectomy, or by intradiscal ozone injection. Acta Neurochir Suppl. 2005;92:139-142. 178. Wu Z, Wei LX, Li J, et al. Percutaneous treatment of non-contained lumbar disc herniation by injection of oxygen-ozone combined with collagenase. Eur J Radiol. 2009;72(3):499-504. 179. Felder-Puig R, Gyimesi M, Mittermayr T, Geiger-Gritsch S. [Chemonucleolysis and intradiscal electrothermal therapy: what is the current evidence?]. Rofo. 2009;181:936-944. 180. Bo W, Longyi C, Jian T, et al. A pyogenic discitis at C3-C4 with associated ventral epidural abscess involving C1-C4 after intradiscal oxygenozone chemonucleolysis: a case report. Spine. 2009;34:E298-E304. 181. Gazzeri R, Galarza M, Neroni M, et al. Fulminating septicemia secondary to oxygen-ozone therapy for lumbar disc herniation: case report. Spine. 2007;32:E121-E123. 182. Kanai A. Treatment of lumbar disk herniation by percutaneous intradiscal high-pressure injection of saline. Pain Med. 2009;10:76-84. 183. Gerszten PC, Welch WC, King Jr JT. Quality of life assessment in patients undergoing nucleoplasty-based percutaneous discectomy. J Neurosurg Spine. 2006;4:36-42. 184. Manchikanti L, Derby R, Benyamin RM, et al. A systematic review of mechanical lumbar disc decompression with nucleoplasty. Pain Physician. 2009;12:561-572. 185. Yan D, Li J, Zhu H, et al. Percutaneous cervical nucleoplasty and percutaneous cervical discectomy treatments of the contained cervical disc herniation. Arch Orthop Trauma Surg. 2010;130:1371-1376. 186. Nardi PV, Cabezas D, Cesaroni A. Percutaneous cervical nucleoplasty using coblation technology. Clinical results in fifty consecutive cases. Acta Neurochir Suppl. 2005;92:73-78. 187. Birnbaum K. Percutaneous cervical disc decompression. Surg Radiol Anat. 2009;31:379-387. 188. Persson LC, Carlsson CA, Carlsson JY. Long-lasting cervical radicular pain managed with surgery, physiotherapy, or a cervical collar. A prospective, randomized study. Spine. 1997;22:751-758. 189. Bhagia SM, Slipman CW, Nirschl M, et al. Side effects and complications after percutaneous disc decompression using coblation technology. Am J Phys Med Rehabil. 2006;85:6-13. 190. Singh V, Manchikanti L, Benyamin RM, et al. Percutaneous lumbar laser disc decompression: a systematic review of current evidence. Pain Physician. 2009;12:573-588. 191. Lee SH, Kang HS. Percutaneous endoscopic laser annuloplasty for discogenic low back pain. World Neurosurg. 2010;73:198-206. 192. Krugluger J, Knahr K. Chemonucleolysis and automated percutaneous discectomy—a prospective randomized comparison. Int Orthop. 2000;24:167-169.

193. Revel M, Payan C, Vallee C, et al. Automated percutaneous lumbar discectomy versus chemonucleolysis in the treatment of sciatica. A randomized multicenter trial. Spine. 1993;18:1-7. 194. Chatterjee S, Foy PM, Findlay GF. Report of a controlled clinical trial comparing automated percutaneous lumbar discectomy and microdiscectomy in the treatment of contained lumbar disc herniation. Spine. 1995;20:734-738. 195. Haines SJ, Jordan N, Boen JR, et al. Discectomy strategies for lumbar disc herniation: results of the LAPDOG trial. J Clin Neurosci. 2002;9:411-417. 196. Haines SJ, Jordan N, Boen JR, et al. Discectomy strategies for lumbar disc herniation: Results of the LAPDOG trial. J Clin Neurosci. 2002;9:411-417. 197. Appleby D, Andersson G, Totta M. Meta-analysis of the efficacy and safety of intradiscal electrothermal therapy (IDET). Pain Med. 2006;7:308-316. 198. Saal JA, Saal JS. Intradiscal electrothermal treatment for chronic discogenic low back pain: Prospective outcome study with a minimum 2-year follow-up. Spine. 2002;27:966-973. 199. Spruit M, Jacobs WC. Pain and function after intradiscal electrothermal treatment (IDET) for symptomatic lumbar disc degeneration. Eur Spine J. 2002;11:589-593. 200. Lee MS, Cooper G, Lutz GE, et al. Intradiscal electrothermal therapy (IDET) for treatment of chronic lumbar discogenic pain: A minimum 2-year clinical outcome study. Pain Physician. 2003;6:443-448. 201. Lutz C, Lutz GE, Cooke PM. Treatment of chronic lumbar diskogenic pain with intradiskal electrothermal therapy: A prospective outcome study. Arch Phys Med Rehabil. 2003;84:23-28. 202. Cohen SP, Larkin T, Abdi S, et al. Risk factors for failure and complications of intradiscal electrothermal therapy: A pilot study. Spine. 2003;28:1142-1147. 203. Davis TT, Delamarter RB, Sra P, Goldstein TB. The IDET procedure for chronic discogenic low back pain. Spine. 2004;29:752-756. 204. Gerszten PC, Welch WC, McGrath PM, et al. A prospective outcomes study of patients undergoing intradiscal electrothermy (IDET) for chronic low back pain. Pain Physician. 2002;5:360-364. 205. Freedman BA, Cohen SP, Kuklo TR, et al. Intradiscal electrothermal therapy (IDET) for chronic low back pain in active-duty soldiers: 2-Year follow-up. Spine J. 2003;3:502-509. 206. Sharma SK, Jones JO, Zeballos PP, et al. The prevention of discitis during discography. Spine J. 2009;9:936-943. 207. Osti OL, Fraser RD, Vernon-Roberts B. Discitis after discography. The role of prophylactic antibiotics. J Bone Joint Surg Br. 1990;72: 271-274. 208. Langer RD, Usmani A, VAN Gorkom KN, et al. In vitro assessment of the antibiotic efficacy of contrast media and antibiotics and their combinations at various dilutions. Br J Radiol. 2010;83:394-400. 209. Willems PC, Jacobs W, Duinkerke ES, De Kleuver M. Lumbar discography: should we use prophylactic antibiotics? A study of 435 consecutive discograms and a systematic review of the literature. J Spinal Disord Tech. 2004;17:243-247. 210. Carragee EJ, Chen Y, Tanner CM, et al. Can discography cause longterm back symptoms in previously asymptomatic subjects? Spine. 2000;25:1803-1808. 211. Simmons JW, Emery SF, McMillin JN, et al. Awake discography. A comparison study with magnetic resonance imaging. Spine. 1991;16(suppl 6):S216-S221. 212. Jackson RP, Becker GJ, Jacobs RR, et al. The neuroradiographic diagnosis of lumbar herniated nucleus pulposus: I. A comparison of computed tomography (CT), myelography, CT-myelography, discography, and CT-discography. Spine. 1989;14:1356-1361. 213. Guyer RD, Collier R, Stith WJ, et al. Discitis after discography. Spine. 1988;13:1352-1354. 214. Fraser RD, Osti OL, Vernon-Roberts B. Discitis after discography. J Bone Joint Surg Br. 1987;69:26-35. 215. Milette PC, Melanson D. A reappraisal of lumbar discography. J Can Assoc Radiol. 1982;33:176-182.

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482  Spine 216. Colquhoun J. The role of lumbar discography in diagnosis of lumbar spine lesions. Orthop Rev. 1977;6:51-56. 217. Patrick BS. Lumbar discography: a five year study. Surg Neurol. 1973;1:267-273. 218. Collis Jr JS, Gardner WJ. Lumbar discography. An analysis of one thousand cases. J Neurosurg. 1962;19:452-461.

219. Kim KS, Yoon ST, Li J, et al. Disc degeneration in the rabbit: a biochemical and radiological comparison between four disc injury models. Spine. 2005;30:33-37. 220. Carragee EJ, Don AS, Hurwitz EL, et al. Does discography cause accelerated progression of degeneration changes in the lumbar disc: A tenyear matched cohort study. Spine. 2009;34:2338-2345.

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Rodney Jones, MD The human experience of chronic pain is a complex bio-­psychosocial disorder and effective management requires concerted effort from multiple sources. Implanted pain therapy devices have gained significant popularity as useful adjuncts in managing severe chronic pain. Spinal cord stimulator and implanted intrathecal drug delivery devices are particularly successful when used in conjunction with other therapy services, procedures, counseling, surgical interventions, and medications. The use of spinal cord stimulation and implanted intrathecal drug infusion for managing chronic pain and spasticity offers distinct advantages and challenges. Both therapies are considered reversible and minimally invasive. Sufficient surgical skill and clinical knowledge required for successful implantation and long-term management by the skilled physician can be learned in a proctored environment with diligent study and dedication. This chapter will discuss spinal cord stimulation and implanted intrathecal drug infusion devices and offer some guidance on patient selection, trial processes, permanent implantation, operative procedures, and postimplant patient management.

Spinal Cord Stimulation Passing an appropriately configured low voltage alternating current through the dorsal spinal cord can induce a tingling or “pleasant paresthesia”. When this generated paresthesia covers or overlays areas of pain, the paresthesia it is said to be “concordant” with the pain. This concordant paresthesia may substantially reduce the perception of pain and is the goal of spinal cord stimulation (SCS) therapy. This reduction in pain perception is often maintained for prolonged periods lasting years if appropriately managed. The use of electricity to mitigate the experience of pain is long and varied in human history. After Melzack and Wall’s 1965 publication in Science,1, in which they proposed the gate control theory of pain reduction, there appears to have been renewed interest in electricity as an adjunct in pain management. Transcutaneous nerve and muscle stimulation has enjoyed a long history of use.2 The effectiveness of these devices for managing chronic pain is debated.3,4 Spinal cord stimulation as a modern pain management practice was introduced by Shealy and colleagues in 1967.5,6 Shealy reported reduced pain in a patient by placing electrodes in the intrathecal space adjacent to the dorsal column of the spinal cord. Various mechanisms of spinal cord stimulation have been proposed and remain an area of ongoing research. Likely, multiple mechanisms play a role.7,8-15

Current spinal cord stimulator systems consist of an epidural array of contacts and a power source or “pulse generator”. Typically patients are afforded a trial period during which the pulse generator is an external device connected to percutaneously inserted epidural electrodes. When the system is permanently implanted, the power source is surgically implanted into a subcutaneous pocket and is called an implanted pulse generator (IPG). Various stimulating parameters are adjustable on both external and internal power sources and represent the “programming” aspect of spinal cord stimulator management. For both trial and permanent implantation, electrode arrays are implanted into the epidural space as either “catheter-” or “paddle”-shaped devices. The catheter-shaped electrode or “percutaneous lead” is inserted through a specially configured needle-type introducer. The introducer is advanced into the epidural space utilizing fluoroscopic guidance and typically with a loss of resistance technique. The introducer may be inserted through the skin (percutaneous) or placed after an incision is made. One or more percutaneous leads are implanted to create the epidural array of metal electrode contacts. “Paddle” electrodes or laminotomy leads are much larger plastic substrate devices to which multiple metal electrode contacts are attached in various configurations. Figures 41-1 and 41-2 are images of current Medtronic and St. Jude Medical (Advanced Neuromodulation Systems, Inc. [ANS]) percutaneous and laminotomy leads. Because of their size, paddle electrodes require laminotomy or laminectomy for placement. Early electrode arrays were 2 or 4 contacts and available power sources contained only non-rechargeable batteries or required an inductive coil held over an implanted receiver coil for continuous power. At this writing, implanted power sources are capable of connecting up to 16 contacts and contain rechargeable or non-rechargeable batteries. ­Figures 41-3 and 41-4 are images of Medtronic and St. Jude Medical (ANS) implanted pulse generators. Often, two and on occasion three percutaneous leads are implanted to create an array of contacts, whereas paddle leads have 4, 8, or 16 contacts arranged in various configurations of columns and rows. Electrode arrays are most commonly placed in the epidural space between the second cervical and the eleventh thoracic vertebra levels over the middle portion of the cord. Retrograde electrode placement to stimulate sacral and lower lumbar nerve roots, lateral lead placement to stimulate nerve roots within the spinal canal, peripheral nerve stimulation, and subcutaneous “field” stimulation16 are all areas of ongoing investigation.17,18 This discussion is limited to traditional “dorsal column” stimulation, which represents the most common current usage of the SCS equipment. 483

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Figure 41-1  Medtronic percutaneous and laminotomy leads. (Reprinted with the permission of Medtronic, Inc. ©2010.)

Figure 41-3  Medtronic rechargeable IPG with percutaneous leads connected. (Reprinted with the permission of Medtronic, Inc. ©2010.)

Figure 41-2  St. Jude Medical (ANS) percutaneous and laminotomy leads.

Indications Appropriate patients for SCS would include those whose pain is not acceptably managed with less invasive therapies and those for whom a definitive surgical procedure is not offered or is not desired.19 Often reserved for use later in a pain management continuum, spinal cord stimulation may be offered early in some cases, especially in the management of predominantly neuropathic and complex regional pain. Spinal cord stimulation has FDA indications in the management of pain of the trunk and or limbs. This somewhat nonspecific indication reflects the broad array of painful conditions that have been helped using spinal cord stimulation. Good to excellent long-term pain relief has been obtained in multiple chronic pain syndromes including failed back surgery syndrome (FBSS),20-28 complex regional pain syndrome (CRPS),29-37 postherpetic neuralgia,38-42 and radicular pain secondary to central and foraminal stenosis in the nonoperated patient. Several other painful conditions have been successfully managed with SCS including: pain secondary to inoperable ischemic cardiac pain,43-54 diabetic peripheral neuropathy,55,56 peripheral vascular ischemic pain, and Raynaud syndrome.57,58 Thoracic, abdominal and pelvic pain coverage with SCS has enjoyed only limited success but clinical efforts continue to afford SCS benefits to these patients.59-62 Early in its history, but rarely today, SCS has been used for spasticity management.63-68 The application of spinal cord stimulation in primarily somatic pain conditions is often less successful than when used for radicular or neuropathic pain. Effective long-term axial low back and neck paresthesia coverage is an area of research and significant clinical efforts. Axial pain may often be somatic, neuropathic, or a combination and, as such, is more difficult to capture long term with dorsal column stimulation. However, because the causes of pain can be greatly varied and unknown, patients with a lower probability of success using SCS may derive considerable benefit. The opportunity to place a trial

Figure 41-4  St. Jude Medical (ANS) implanted pulse generators.

stimulator consisting of percutaneously placed electrodes connected to an external pulse generator is a tremendous advantage and is what allows the less-than-optimal patient to be considered.

Contraindications The following situations would generally contraindicate SCS: Known systemic bacterial infection or infection in the proposed implant region ll Patients with an untreated or undiagnosed psychiatric condition ll Posterior surgical interventions that obliterate the epidural space where the lead array needs to be placed or along the required implant path of the lead ll Patients unwilling or unable to comprehend using the device ll Anticoagulated patients where the anticoagulated state cannot be stopped for the trial and implant process69 ll Pregnancy ll Previous DREZ lesions at or above the level of lead placement19,70 ll Deafferentation or CNS damage such that paresthesia generation is not possible71 ll

Spinal Cord Stimulation and Implanted Intrathecal Drug Infusion  485

Significant canal stenosis along the proposed lead location contraindicates percutaneous lead placement and would make laminotomy lead placement in the area of stenosis a concern. Posterior spine surgeries most often obliterate the epidural space and lead placement through the surgical area typically is not possible. Magnetic resonance imaging (MRI), or if MRI is contraindicated, computed tomography (CT) scan of the proposed lead placement regions are often warranted to screen for significant canal stenosis or other intraspinal anomalies.

Equipment At time of this writing, three companies manufacture and support the majority of spinal cord stimulator equipment: Medtronic Neurological, St. Jude Medical (ANS), and Boston Scientific. Each company has product sales and support personnel. Generally, these companies provide a variety of lead or electrode packages containing the electrode, introducer needle, various stylets, and anchors. Percutaneous leads typically have four or eight electrodes secured to a solid plastic catheter through which wires pass to connect the electrodes to metal contacts on the other end to connect to the power source. A trialing cable to connect the leads to a trial pulse generator may be included in the lead kit, or supplied as a separate item. The various implanted pulse generator packages contain a tool for securing the lead to the IPG. Many items are individually packaged and available when needed such as: various anchors, additional stylets, wrenches for the set screws on the IPG or extension, lead extensions, and others. When connecting electrodes placed in the cervical region and many laminotomy leads to an IPG located in the upper buttock or abdominal region, lead extensions are typically required. The basis for all SCS systems is essentially the same: Various forms of a low voltage alternating current are passed from the generator to an array of electrode contacts in the epidural space to generate an electric field within the spinal cord.72-75 This electric field affects a change in the central nervous system and, when effective, the experience of pain. Each company has claims to unique benefits, programmability, battery life, stimulation parameters, constant voltage versus constant current and various equipment features. Implanter experience with the various products, individual bias, possibly geographic location due to product support issues, and experience of the manufacturers support personnel are important when choosing which company or companies to choose. Each manufacturer’s trial and implanted generator is designed to connect only to that particular company’s leads. A battery powered external pulse generator is programmed to match those settings found to be most beneficial during the trialing process and is sent with the patient for the trial period. Trial leads are not appropriate or intended for permanent implantation. Implanted pulse generators are used as the power source for permanent SCS systems. At this writing, IPG power sources are either rechargeable or non-rechargeable (primary cell). An inductive coil IPG was marketed by Medtronic and ANS (St. Jude Medical), but these are generally not used or are out of production. The decision to implant a primary cell powered versus a rechargeable device is made based on expected power requirements as determined during trialing of the array at time of implant, patient cognitive abilities, and implanter preference and experience. Power requirements for a trial implant array do not necessarily always predict requirements for an array placed during a permanent implant. Current Medtronic rechargeable IPGs will stop functioning after 9 years of usage and require replacement at that time. Boston

Scientific and St. Jude Medical rechargeable IPGs do not have specific time limits. The actual life of the rechargeable devices is dependent on the type of battery technology, the number of battery recharge cycles, and the efficiency of the device. As the battery life depletes, the frequency of required recharges increases. A primary cell, non-rechargeable IPG battery under typical usage is expected to last approximately 6 years. Less maintenance from the patient (in the form of recharges) is required with a non-rechargeable IPG. When choosing between rechargeable or non-rechargeable power sources, battery recharging requirements must be weighed against the advantage of the battery’s expected increased life. When power requirements were high during trialing for the permanent electrode placement, then a rechargeable device may be more appropriate. Laminotomy leads tend to have considerably lower power requirements and therefore non-rechargeable power sources may be adequate. In general, however, the greater the power usage, the more likely it will be for a practitioner to choose a rechargeable option.

Preoperative Considerations Preoperative evaluation and preparation of a patient are critical to optimizing outcomes. Most implanters and payers will require a pre-implant psychological evaluation.76-78 This evaluation is best accomplished by a licensed psychologist or psychiatrist who has a clear understanding of issues associated with chronic severe pain and spinal cord stimulation. This evaluation helps the implanting physician identify psychological factors that invariably are present in patients with chronic severe pain. Occasionally, psychological issues are identified that require treatment prior to further consideration of spinal cord stimulator therapy. Good collaboration between the psychologist or psychiatrist and implanting physician is important and that all involved understand and address psychological issues. Long-term psychological needs may also be identified during this evaluation. Mostly the evaluation is an attempt to identify psychological issues that would preclude a patient from being considered for implantation. It is important that this evaluation be obtained before placement of the trial and incorporated in the overall pre-implant decision-making process. An accurate and timely history and physical examination appropriate for a surgical patient is reasonable. This would include past surgeries, surgical complications, bleeding problems, drug allergies, current medications—with specific attention to those affecting coagulation,79,80 and appropriate review of systems. A physical examination related to the proposed procedure would include a focused neurologic examination, auscultation of the heart and lungs, abdominal palpation, and inspection of the proposed surgical sites for evidence of infection. A discussion with the patient and significant others regarding external wires and the trial pulse generator for a trial placement, expected incision locations for permanent implant, expected increased pain, and activity restrictions is prudent. Preoperative laboratory testing may be appropriate to rule out infections, bleeding problems, and chemical abnormalities. Chest radiographs and ECG may also be appropriate in patients with significant cardiac or pulmonary history. Specific tests and studies obtained are determined by individual patient considerations, facility requirements, and anesthesia needs. Identification of possible immune deficiencies and, when indicated, evaluation of the immune status of patients is important. Patients with a history of recurrent infections, especially those known to have antibiotic-resistant organisms, are at particular risk. Diabetics, patients with poor personal hygiene, unsanitary living

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conditions, chronic renal failure, long-term steroid exposure, the elderly and/or debilitated, and most obviously, those with known immunoglobulin deficiencies require careful considerations. When in doubt, consulting an internist and/or infectious disease specialist is appropriate. Maximize immune function in those patients identified to be at risk when possible. Appropriate perioperative antibiotics in the at risk patient and possibly all patients are important in reducing operative infections. Most preoperative antibiotics are best given within 30 minutes prior to incision.

Facility Surgical implantation of permanent SCS systems is a surgical procedure requiring adherence to the usual surgical precautions and needs. Implantation of trial percutaneous spinal cord stimulator leads is generally also considered a surgical procedure requiring similar surgical precautions. C-Arm fluoroscopy is most typically used in addition to an x-ray translucent table, free of metal components which might interfere with appropriate x-ray imaging. Monitoring equipment appropriate for specific patient needs would typically include noninvasive blood pressure, pulse oximetry, and ECG. As with all surgical interventions, a surgery suite meeting local Life Safety Code, conditioned and filtered air, and backup electric power suitable for a surgery suite would be expected. Appropriate monitoring and resuscitation equipment to care for the surgical patient is also required. This would include airway management equipment and supplies, resuscitation drugs, cardiac defibrillator, as well as personnel trained in airway management and patient resuscitation.

Surgical Considerations Typically, for both trial lead placement and permanent system implantation, patients are positioned supine with or without a pillow under the abdomen as needed to reduce lumbar lordosis for lumbar entry. Padding the upper chest will allow the neck to flex for upper thoracic entry when cervical placement is planned. Skin preparation is tailored to patient requirements and may be accomplished by washing the area, shaving when needed with an electric shaver, and final prepping with an applied iodine or chlorhexidine surgical prep. Plastic barrier drapes impregnated with iodine or chlorhexidine applied over the incision and introducer insertion areas will reduce local skin bacterial contamination. Appropriate draping of the patient and equipment including the C-arm is important. Adherence to strict aseptic techniques by all personnel is critical to reducing infections. All room personnel must wear clothing appropriate for an operating room environment with surgical masks and hair caps. As in all implant surgeries, minimizing the handling of the sterile implanted devices lessens the chance of contamination. Liberal antibiotic irrigation may reduce the incidence of infection. Electrocautery is cautiously used by many implanters during the permanent implant process. Never cauterize near the introducer needle because severe shock and damage to the spinal cord may occur. Avoid cautery near any component leads or wires because the current may be transmitted down the wire and shock or damage neural structures. Heat from cautery will damage leads, extensions, and other components possibly causing failure. Cautery current has the potential to damage the electronic components of implanted pulse generators. Some implanters prefer using bipolar cautery to mitigate, but not eliminate, cautery risks. Heat from

cautery damages surrounding tissues, which must go through a healing process. Increased seroma formation, wound healing complications, and infections are noted with excessive cautery usage. Good surgical techniques, with proper wound closures in layers when needed, will reduce wound-healing complications. Additionally, local skin flaps when needed, creation of a generous IPG pocket, and closure of deeper fascial planes will help reduce tension across wound closures, thereby lessening wound healing complications. The use of absorbable suture in deeper layers is typical. A less reactive suture material such as PDS II (polydioxanone) may reduce the incidence of stitch abscess and superficial wound complications. Final skin closure with staples, nylon, or tissue glue such as DERMABOND adhesive may also provide an added level of skin approximation. Unlike nonimplant surgical procedures, superficial skin infections and wound healing complications may lead to involvement of deeper layers, exposing the implanted devices to infection. When deeper layers of the back incision or the pocket become infected, very often the entire system must be explanted to appropriately treat the infection.

Trial Process Considerations The implantation of electrodes on a trial basis offers the patient, caregivers, and managing physician an opportunity to evaluate the effects of spinal cord stimulation prior to permanent implant consideration. Meaningful application and evaluation of the trial process is a combination of patient expectations, physician and staff experience, proper lead placement, programming of the electrode array, and careful evaluation of the stated results. As with many therapies, there is a substantial placebo response which must be considered when evaluating patient response to a trial of spinal cord stimulation. Concordant paresthesia generated over the area of pain, which is reported by the patient to significantly reduce pain perception, is the goal of the trial. The length of time the trial leads remain implanted varies among practitioners and mitigating issues such as the need for anticoagulation medications and immune status. Most generally, the trial period should be long enough to allow the patient to use the stimulator while engaging in their usual activities of daily living. Typically, the trial duration is 5 to 14 days. Some practices occasionally use an “on the table” trial where the system is permanently implanted if the patient reports good relief with initial lead placement. This practice is most appropriate in situations where percutaneous lead placement is not possible and a laminotomy is required. An experienced implanter assesses the reported paresthesia and considers the risks and benefits of immediately implanting the permanent system. Permanent implantation of a laminotomy lead connected to an extension passed through the skin and attached to a trial generator has been used. An IPG and new extension can later be implanted if the trial is successful. Long-term success of spinal cord stimulation cannot be completely predicted by the trial process. Positive placebo response with a trial implant can lead to poor permanent implant results. A positive placebo benefit will lessen over time and may account for many early nonimplant-related failures that appeared to have initially functioned well. If the trial protocol requires a very high reported level of benefit before a permanent implant is offered, improved long-term success would generally be expected. For example, patients who report only a 40% reduction in pain may be experiencing significant placebo response, and may not be the best candidates for permanent implantation. Factors to consider in

Spinal Cord Stimulation and Implanted Intrathecal Drug Infusion  487

the determination as to the effectiveness of the trial would include reported effects such as increase in activities of daily living; reduction in oral pain medication usage; family members reporting improvement in activities and mood; improved sleep pattern; and a reported decrease in level of pain during activities and at rest. Unfortunately, even in the best of circumstances, placebo response cannot be completely controlled. Some permanent implantations will not be successful and will rapidly lose effectiveness secondary to waning placebo response. Keeping the expected level of benefit from the trial high and the duration long will help mitigate placebo response. However, consideration should be given that by using a strict protocol requiring a very high level of relief during the trial (i.e., greater than 80%), some patients will be denied spinal cord stimulation that could otherwise benefit. The trial process has great impact on an individual patient and is the patient’s critical opportunity to gather information to make an informed decision whether to continue to permanent implant. Considerable care must be given to this very important process. Preprocedure education, expert psychological evaluation, and careful discussion with all concerned regarding the process and expectations will help reduce disappointment and failure. Poor lead placement and/or programming that fails to provide optimal paresthesia coverage is not acceptable and will doom the trial from the beginning. For the patient’s benefit, effort must be given to provide as good a trial as is reasonably practical. Percutaneous trial leads are placed through needle type introducers inserted through the skin. Lead location is adjusted based on the patient’s reported paresthesia when the lead is connected to a trial generator. The trial leads may be secured using various techniques. Figures 41-5, 41-6, and 41-7 demonstrate one method whereby the leads are sutured to the skin with 0-silk, tincture of benzoin applied and Steri-Strips are placed to create a loop of lead to act as a strain relief. A 4 × 4 dressing is applied and secured with wide 3M Medipore H tape. The trialing cable is also secured with tape to reduce stress at the lead cable connection. In the recovery area, final adjustments are made to the trial generator parameters when needed, and instructions are given to the patient and caregivers. Although use of the trial generator is

Figure 41-5  Securing percutaneous leads with 0-silk.

straightforward, considerable time may be needed to assure and instruct the patient and care givers in its use. The patient is most frequently discharged to home and given instructions including a contact number to call when questions arise. Patients are cautioned against twisting and bending movements which might cause the leads to move from their implanted location. However, the patient is encouraged to engage in usual activities of daily living as practical to best assess the stimulator’s effectiveness. Although a reduction in pain medication requirements is one indication of effectiveness, if pain medication is abruptly discontinued during the trial implant, confusion may arise as to effectiveness. Patients are asked not to get the dressings wet and to contact the physician for any dressing changes that may be needed. After completion of the trial, the patient and care givers are questioned regarding perceived benefits, and if a pain diary was kept, it is reviewed. The percutaneous trial leads are most generally removed by gentle traction on the lead with the patient in a slightly flexed sitting position. If unusually severe or radicular pain

Figure 41-6  Tincture of benzoin and Steri-Strips with a strain relief loop.

Figure 41-7  Gauze dressing and Medipore tape to secure the dressing and trial cable.

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is experienced when attempting removal, the patient is repositioned prior to further attempts. A successful trial is defined differently by various physicians. Most physicians consider at least a 50% reduction in pain, improvement in activities of daily living, and some medication reduction to be important. The determination to proceed with permanent implant may best be delayed for several days following removal of the trial. This period without the SCS effect allows time for comparison and gives the patient and physician additional information. It is important that the patient, care givers, and family members have reasonable long-term expectations. Clear understanding of the surgical implant process including short and long-term risks as well as postimplant requirements is important. The patient is made aware of the possible need for further surgeries for lead revision, equipment failure, and eventual IPG replacement.

Percutaneous Lead Placement Lead placement whether for trial or permanent system implantation is preformed using minimal, if any, conscious sedation with appropriate amounts of local anesthetic. Moderate or heavy sedation is discouraged to lessen complications associated with introducer placement and lead advancement. Reported paresthesia location, quality, and benefit by overly sedated patients are suspect and difficult to interpret. Paresthesia qualities will often change as the level of sedation lessens. Clear verbal communication with the patient is critical during the lead placement process. Lingering sedation given for local infiltration, incision, introducer placement, and lead advancement can significantly affect the patient’s perception and reported paresthesia. Reassuring words along with slow infiltration of reasonable quantities of local anesthetic solutions into the appropriate region will greatly reduce sedation requirements. In permanent implantation, when the leads are anchored and trialed to ensure an appropriate stimulation pattern, patient communication becomes less important and increased sedation, if needed, can be given. Percutaneous leads are inserted through a specially designed large-bore (approximately 14 gauge) introducer needle. These introducers allow leads to emerge from the tip, to be advanced and carefully manipulated during the placement process. Leads can be damaged and even sheared while withdrawing through the introducer. When there is resistance to withdrawal, slight advancement and rotating the lead may allow the lead to be successfully withdrawn. When there is concern that damage to the lead may occur, removal of the introducer and lead together with subsequent reinsertion of the introducer is indicated. For lumbar radicular pain, the expected region of the spinal cord best stimulated typically will reside between the sixth and eleventh thoracic vertebral level. Needle entry would be at T12-L1 or L1-2 when practical. Motion within lower lumbar segments may increase lead failures such as fracture and dislodgment. For cervical lead placement, introducer insertion at C7-T1 or below is best—again due to motion and typically a more generous epidural space. Cervical lead tips are positioned somewhere below the C2 level. The spinal area being considered for placement of the introducer needle is imaged most generally with C-arm fluoroscopy. The C-arm is adjusted in oblique and tilted projections to provide an optimal view of the intended entry interspace. Inspection of the interspace may reveal boney changes that could make introducer placement or subsequent lead advancement difficult. Often, declining the fluoro beam to more closely match the needle entry angle

can demonstrate obstruction or anatomic variations. Paramedian insertion of the introducer needle is preferred starting approximately one spinal level below. The entry angle of the introducer relative to the spine should be approximately 45 degrees when practical to allow for the lead to optimally emerge from the tip. This angle also improves the ability to “steer” or to control the lead tip as it is advanced. The introducer tip target is slightly ipsilateral and below the spinous process. Figure 41-8 shows a left paramedian introducer placement at T12-L1. Air or saline loss of resistance technique is most often used along with anterior-posterior and lateral fluoroscopy imaging as the needle is advanced to assist in identifying the epidural space. Nonionic contrast may also be employed if needed to help confirm epidural space placement. Most introducer placements are at spinal levels where the spinal cord is present. Great care is exercised to have exacting needle control as the introducer is advanced so as not to cause damage to the spinal cord. Figure 41-9 demonstrates one technique of holding the syringe and needle. Notice the operator’s left thumb and index fingers grasping the needle at the skin level while the right hand gently “bounces” the syringe plunger providing pressure for the loss of resistance. The introducer is advanced only by the fingers pinching the needle while the right hand assists in directing the introducer. Using this technique, the introducer is less likely to be accidentally advanced into the dural space possibly causing spinal cord or nerve root injury. Once the introducer is in place, an electrode or lead is inserted through it and advanced staying midline or slightly off midline to a level above the expected final implant level. When practical, it is best that the electrode emerge from the introducer directly cephalad and not angled to either side. Fig. 41-10 demonstrates the lead emerging from the introducer directed cephalad. Lumbar and thoracic leads can easily stray laterally when advanced and pass laterally and then into the anterior epidural space where paresthesia is not pleasant. Depending on implanter experience and

Introducer

Rt

Figure 41-8  Proper introducer placement using a left paramedian approach at the T12-L1 interspace. This patient has a fusion of L3 and below.

Spinal Cord Stimulation and Implanted Intrathecal Drug Infusion  489

the desired paresthesia, the lead may be placed directly midline or slightly off midline. Once the lead is initially placed, it is connected to a trial generator using a cable passed from the sterile field. Some of the lead contacts are selected, for example, three in the middle portion on an eight contact electrode, in a +,−,+ configuration. The power is increased on the trial generator until the patient reports tingling or paresthesia, which they are asked to describe. The lead is slowly withdrawn while the patient reports changes in the quality and location of the paresthesia. If in this process a very good paresthesia is obtained, which the patient assuredly reports to be beneficial, the lead may be left at that location. When the lead is withdrawn to a spinal level at which useful paresthesia is no longer reported, the lead is advanced back into a position where the most optimal paresthesia was reported. These position adjustments are made slowly

Figure 41-9  Exact needle control during introducer placement. Advancing only with the left thumb and index finger.

and in cooperation with the person controlling the trial generator to minimize unpleasant or very strong stimulation. This “trolling” technique can reduce the number of adjustments required for optimal final lead placement. Trial generator parameters may be adjusted as needed to improve paresthesia coverage, but finetuning of the parameters for optimal coverage is generally undertaken at a later time. Generator parameters include pulse width, frequency, power (voltage or current), and lead contact configuration (each contact can be set to +, −, or off ). If on initial trialing, the patient reports a sharp biting pain at a very low power setting, the lead may be intrathecal. The lead is withdrawn and an attempt may be made to reinsert at this or a different level. On occasion, CSF in the epidural space from a dural puncture by the introducer may make trialing the lead difficult because the CSF interferes with the conductance. In this situation, the procedure is best abandoned and again tried at a later date. If the lead is being placed in the thoracic region, and the patient reports sharp pain within the chest wall or abdomen, the lead may be in the anterior epidural space or lateral in the posterior epidural space stimulating the nerve roots. A lateral fluoroscopic image is often useful in diagnosing these placements. Stimulation of the ligamentum flavum may be reported as a sharp or biting posterior sensation as the power is increased.81 Repositioning of the lead may reduce this undesired stimulation. Implantation of laminotomy leads in lieu of percutaneous leads is thought to reduce this ligamentum stimulation. Many implanters repeat this lead implantation process with additional leads to provide optimal paresthesia coverage and afford more programming flexibility.82 With changes in pain patterns, electrode movement, and scar formation, reprogramming with multiple contacts is generally more successful. Two percutaneous leads are generally placed in this fashion to provide an electric field across the spinal cord. Occasionally, three electrodes are implanted and are thought to possibly offer some advantage from a “tri-pole” electrical field.83 Fig. 41-11 is an AP radiograph showing

T9

Rt

Rt Lead emerging from introducer

T12 T12

Figure 41-10  Lead emerging from introducer directed cephalad slightly left of midline.

Figure 41-11  Anteroposterior (AP) radiograph of a dual percutaneous lead array prior to introducer removal.

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Two leads in posterior epidural space

Tip of introducer

Figure 41-13  Anchoring lead to fascia. L2

Figure 41-12  Lateral projection of two percutaneous leads with one introducer in place.

the electrode positions following trialing but before the introducers were removed and Figure 41-12 shows a lateral projection of the same leads after one introducer was removed. The epidural space contains nerve roots, fat, connective tissue, lymphatics, venous vessels, and small arteries. These small arteries supply posterior spinal structures and do not supply the spinal cord. Tissue adhesions within the epidural space may make passage of the electrode more difficult. When a patient is in the prone position, contact between the ligamentum flavum and the dura may be less consistent. Tissues contained within the epidural space may reduce effective contact between the dura and the electrode. Often stimulation is stronger when the patient lies supine owing to improved electrode contact and the spinal cord’s posterior movement ­secondary to gravity.

Surgical Implantation of Percutaneously Placed Leads When permanent percutaneous leads are placed, a midline incision at the expected lead implant spinal level may be made prior to placing the needle introducer(s). The advantage of this technique is that good exposure of the spine and hemostasis using cautery can more easily be accomplished prior to introducer placement. The disadvantage is that the incision may need to be extended when placement at the expected level cannot be accomplished or when a more lateral introducer insertion is required. Incisions may be made following placement of the leads through the skin. If the leads are placed in a bilateral paramedian approach, the incision is made between them. If they are placed on the same side, the incision is made alongside both introducers. Some implanters make a separate incision at each introducer location. When making two or more incisions, consideration must be given to wound healing complications owing to impaired blood supply to the skin areas between incisions. The dissection is made to the fascia overlying the spinous

process and developed as needed for exposure. Dissection to the entry point of the introducer into the spinal fascia or ligament is required when the leads are placed percutaneously prior to incision. Following careful removal of the needle, the lead is drawn backwards through the skin puncture into the incision and anchored. When the incision is made prior to introducer placement, cautery may be used before introducer placement. Lead movement from the initial implant location is the most common cause of lead failure. This typically arises from failure at the anchor. Leads can move laterally or medially without failure at the anchor site. Device companies have made good progress in developing new anchors that securely hold the lead with minimal circumferential pressure. Proper use of anchors, referencing manufacturer technique recommendations, and suturing to appropriate structures are critical to long- and short-term success. The anchor is generally sutured along the posterior lateral aspect of the spine, such that the leads are not sharply bent. This reduces stress points that can cause failure of the internal wires. Anchors are applied as close as practical to the point where the lead enters the interspinal ligament or fascia. Figure 41-13 shows an anchor sutured at each end and a tie being passed around the anchor to apply circumferential pressure securing the lead to the anchor. Leads may pull back with spinal flexion-extension movement and emerge between the fascia entry point and the anchor, especially if this distance is great. A nonabsorbable, purse-string suture placed around the introducer needle prior to removal and tightened after final verification of lead position may reduce this complication. Stress points along the leads are reduced by providing room for them to coil and to lie flat within tissue planes. Generally, a flap of skin or deeper tissue is developed in the inferior aspect of the incision to allow the lead to curl in this area and provide strain relief.

Permanent Laminotomy Lead Implantation Laminotomy or surgical leads are also referred to as paddle leads because of their shape. A laminotomy or laminectomy is generally required to provide enough room for insertion into the epidural space. Electrode contacts reside on the surface toward the spine and are, therefore, insulated on the posterior surface. Generated electric fields with these leads are unidirectional toward the dura and spinal cord. The posterior surface against the ligamentum flavum

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41

Figure 41-14  Minimally invasive laminotomy lead placement.

is insulated, so stimulation of the ligament is unlikely. These leads tend to be more efficient and require less power to produce paresthesia. Current laminotomy leads have 4 to 16 contacts arranged in various configurations of contact size, spacing, and orientation. It is likely that their larger size makes them less prone to movement when implanted. The placement of paddle electrodes may be accomplished using minimally invasive spinal retractors and access systems or via a traditional open laminotomy.84 Figure 41-14 shows a laminotomy lead being implanted using a minimally invasive technique. To confirm useful concordant paresthesia, the patient is questioned during trial stimulation whenever a lead array is being implanted. Intraoperative questioning requires the laminotomy be performed using spinal or epidural block and local anesthesia infiltration with sedation when required.85 Spinal and epidural block anesthesia along with local anesthesia infiltration can be used when correct paresthesia reported.86 The location of optimal laminotomy lead placement can often be well approximated by a previously performed percutaneous trial. When the laminotomy lead is placed under general anesthesia at the level as determined by the trial, a risk is taken that, upon patient awakening, less than optimal coverage will be afforded. Figure 41-15 shows a tripole laminotomy lead implanted slightly right of midline.

Figure 41-15  Laminotomy tripolar lead.

Radiation Safety Considerable radiation exposure may be had by the implanting physician during introducer placement and lead manipulation. This is especially true during the early phases of learning. Techniques used to reduce radiation exposure include using a modern C-arm fluoroscopy machine in the pulse and low-dose modes when appropriate; using collimation to view only those areas needed to be imaged; using AP imaging with the x-ray source under the patient; keeping hands out of the x-ray beam; positioning the image so that the area of interest is at the bottom of the image screen; lowering the image intensifier as practical; and proper lead shielding of the surgeon. Proper lead shielding includes leaded goggles to protect the eyes; thyroid shield; full lead apron; and lead batons hanging from the side of the table. A piece of lead sheeting may be fashioned to provide an area of minimal radiation to protect the hands. This shield is sterilized and laid over the drapes. All these maneuvers play a role in reducing lifetime radiation exposure. With practice and experience, typically radiation exposure becomes much less. Figure 41-16 shows fluoroscopy positioning, lead apron, thyroid shield, lead eye protection, and the use of a sheet of lead to

Figure 41-16  Radiation shielding for lead manipulation.

protect the hands. Some of these efforts will also reduce radiation exposure to the patient.

Pocket Creation and IPG Implantation After placement of the epidural lead array, a subcutaneous area or pocket is created to accommodate an IPG. Following infiltration of the proposed pocket area with local anesthetic containing epinephrine to reduce bleeding, a horizontal incision is made to the subcutaneous fat layer. Blunt finger dissection and electrocautery is used inferior to the incision to develop a pocket. Pockets are most often

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Figure 41-17  Tunneling rod placed from back incision to the implanted pulse generator (IPG) pocket.

developed in the upper buttocks just lateral to the upper sacrum. This area typically is below the belt line and pressure against a chair is minimal. Smaller power sources may allow for a suitable pocket to be developed adjacent to the lead implant spinal incision. Recharging may be more difficult with the IPG in these areas and should be considered when planning pocket location. Other IPG pocket sites include the abdomen or infraaxillary region. Placement under muscle or a fascial layer may be needed in extremely thin patients. The pocket is usually developed inferior or below the incision such that the incision does not overlie the IPG. Rechargeable IPG pockets are best created under less subcutaneous tissue to reduce the distance between the IPG device and the recharging coil placed over it. Device company recommendations are followed in regard to pocket configuration and depth. If a non-rechargeable device is implanted, pocket depth can generally be greater—but not so great as to make communicating with it difficult. A tunneling device is inserted through the subcutaneous tissues and passed between the pocket and the spine incision. The leads or lead extensions when required are passed or drawn into the pocket. Figure 41-17 shows tunneling between the spinal incision site and the IPG pocket. Connections are carefully dried and secured to the IPG using a special tool. Most IPGs have two suture holes along the upper edge where nonabsorbable sutures are used to secure the IPG to a fascial plane. These sutures keep the IPG from turning in the pocket. Rotation and movement of the IPG in the pocket over time will stress the lead wires causing fracture and lead dislodgement. These sutures are best placed through a deep fascia layer and tied with 2 to 3 cm of slack. Figure 41-18 shows the IPG with silk sutures being placed. Figure 41-19 shows how placing an instrument into the loop of tie will allow the knots to be tied tightly while leaving slack in the loops to reduce failure. If these sutures are tied tightly, they tend to “saw” through the tissues over time and fail. The spinal incision and the pocket are closed with absorbable sutures in layers when appropriate.

Postoperative Measures Postoperative instructions include antibiotic coverage, dressing changes, wound care, pain medications, symptoms and signs for the patient to be vigilant of and for which the physician should be

Figure 41-18  Suturing IPG into Pocket.

Figure 41-19  Tying the implanted pulse generator (IPG) sutures with an instrument in the loop to provide slack.

notified. For trial placements, the dressing may be left in place until the trial leads are removed. If a trial lead dressing becomes soiled or wet, dressing change by the physician or staff would reduce incidence of damage or lead dislodgement. After surgical interventions, including permanent implants, system removal or revisions, dry gauze type dressings taped in place with nonplastic tape works well. Over time, occlusive dressings may hold moisture and become sites for bacterial entry. Patients implanted with permanent devices are instructed not to get the dressing wet; no soaking in water for a period of at least four weeks is recommended. Wrapping plastic kitchen wrap circumferentially around the low abdominal and midback regions will allow patients to shower without compromising the dressing. Otherwise, sponge bathing may be best. If the dressing becomes wet or soiled, it is to be changed. Wounds are cleansed only with mild soap and water or dilute hydrogen peroxide. Antibiotic ointments are avoided as this may introduce ointment into deep layers, impairing skin approximation and healing. Antibiotics are provided during the trial period and after permanent system implantation or revision according to the implanting physician’s experience, patient needs, and type of surgery. For the average-sized adult, an antibiotic such as Keflex (cephalexin), 500 mg PO, q 6 to 8 hours unless patient is allergic or allergic to a

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typically cross-allergic antibiotic is appropriate. For patients with impaired immune response or known chronic infections, consultation with an infectious disease specialist may be appropriate. Patients may require additional pain medications. For trials, this would be minimal and care is given not to increase the amount to such a level as to impact the trial results. Some added discomfort may be expected for 1 to 2 days following a difficult percutaneous lead placement due to introducer placement. After this period, an attempt is made to return the patient to their baseline pain medications or even a reduced dose. In permanent system implantation, surgical pain is expected and may be considerable during the first 2 to 3 postoperative days. Increased pain medication requirement during the first week would be expected. Adding transdermal fentanyl for this postoperative pain is not appropriate and is avoided unless the patient had been using transdermal fentanyl as part of their general pain management regimen. Activity is limited following permanent lead placements. Aggressive spine twisting and bending motions are discouraged for 6 to 8 weeks after which the leads are thought to be held in position by scar forming around the lead in the epidural space. Trial leads are left in place only days and during this brief period, significant scaring of the leads will not develop. Part of the trial process, however, is to encourage patients to engage in their usual activities. These activities may, of course, cause leads to move from their implanted locations and patients are counseled regarding this possibility. If trial leads move after sufficient time has elapsed, such that the patient can make a reasonable determination of effectiveness, then the trial need not be repeated. However early lead movements to a point where reprogramming is unable to regain paresthesia, may necessitate repeating the trial. Patients often report significant increased stimulation during acceleration in automobiles owing to improved contact and the cord moving closer to the electrodes. Therefore patients are advised not to drive with the stimulator ­powered on. Postoperative instructions include some counseling regarding possible adverse events. Epidural hematoma occurs most often early with epidural abscess occurring somewhat later after implant and developing more slowly.87

Programming The trial generator and implantable pulse generator (IPG) have multiple programmable parameters. The IPG is programmed through the skin using a wireless device where the trial generator is external and can be directly programmed. Often programming and reprogramming of the IPG by the physician is assisted by a representative of the device company or other knowledgeable staff. After initial IPG parameter settings are programmed, future adjustments are expected in permanent systems due to minor lead movements, scar formation, or pain profile changes. During the trial period, reconfiguration of the trial generator settings may be required if stimulation pattern substantially changes. Each device company has their individual programming system to communicate with the IPG for this programming or reprogramming. A trial generator connected to the lead array by means of a cable passed from the sterile field, is used intraoperatively for the trialing of leads. This is the case whether the lead is being placed for a trial or for permanent implantation. Each contact on the lead may be individually programmed to positive (+), negative (−), or (off ) to not be used. The voltage or current range (amplitude), pulse frequency in hertz (Hz), and pulse width (microseconds) can be

modified to generate the most effective paresthesia. At time of this writing, pulse generators can control as many as 16 contacts, which when adjusted with these various parameters, can create a nearly endless number of possible combinations. Experienced and knowledgeable physician and personnel are needed to optimally program these devices. Various electrode contact configurations along with other parameters are selected and the power is slowly increased while the patient reports specific paresthesia for that particular combination. Based on the location and quality of the reported paresthesia, changes are made to the programming and the power is again slowly increased. This process is repeated until the optional coverage is reported. This process may be time consuming to optimize all reasonable combinations, but with experience it is often manageable.

Complications As with any surgical procedure, even in the most competent of hands, complications will and do occur. The frequency and severity of complications will vary depending on multiple factors, some of which can be mitigated. Severe complications are rare, but can include death, spinal cord injury, or nerve root injury that may occur during the placement of the introducer needle and passing the lead. Short-term complications tend to be related to, and associated with, the implant surgical procedure. Wound healing complications include subcutaneous infection, wound dehiscence, stitch abscess formation, and deep infections. Most infections related to the surgical implant will develop in the first 4 weeks following surgery. If at any time the wound breaks down (dehisces) such that implanted components are visible, aerobic and anaerobic wound cultures must be obtained to help guide antibiotic coverage and to determine if the wound is infected or if mechanical factors led to the dehiscence. Typically, some skin contamination in a dehisced wound is cultured. If the wound is infected, most generally the system is explanted, the infection is cleared, and the patient is later evaluated for possible reimplantation. If wound dehiscence is caused by failure of the closure and the wound is not infected as determined by cultures, surgical excision of the affected skin margins, vigorous irrigation with antibiotic or dilute Betadine (povidone—iodine) solution, and secondary wound closure with PDS-type suture may be attempted. Local skin flap development will reduce the stress across an incision and lessen the incidence of dehiscence. Figure 41-20 shows a dehisced wound being marked for excision of the margins for secondary closure. The cultures and Gram stain along with clinical impressions suggested that this pocket was not infected. Abscess formation around suture material may remain limited to the subcutaneous tissue or can extend and enter deeper layers. When the device capsule is involved or if the deeper layers around a lead implant site are involved, resolution in the presence of the implanted devices is difficult. Epidural Abscess and Hematoma Prompt recognition and treatment of these potentially devastating complications are important. Pain (out of proportion of expected) at or below the level of the lead placement, motor or sensory loss significantly above preimplant level, fever, and chills will prompt concern. If suspicion exists for epidural abscess or hematoma in the trial patient, prompt removal of the trial leads and MRI of the spine at the appropriate spinal levels is performed. In the permanently implanted patient, CT of the appropriate spinal levels and if needed CT myelography may demonstrate an abscess or

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leads results in less-than-optimal data and may require repeating the trial. If trial or permanent leads have moved a minimal amount, reprogramming may be able to adjust for the changes. If reprogramming of a lead array is unable to recapture the desired paresthesia, often surgical lead revision is required. With trial leads, the trial may need to be repeated depending on sufficiency of data prior to lead movement. Tunneling Damage Damage to structures from tunneling can occur and would be expected more frequently when connecting cervical electrodes with generators located in the upper buttocks. The long tunneling distance and possible loss of positive control of the tip of the tunneling device may result in perforation of nearby structures. Pleural cavity and intraabdominal penetration as well as injury to vascular and neural structures is possible. Intraabdominal penetration is greater when the generator is placed in the anterior abdominal area requiring tunneling around the flank.

Figure 41-20  Skin of dehisced implanted pulse generator (IPG) pocked wound marked for excision.

hematoma with cord compression. Currently, all device manufacturers do not approve of MRI scanning at the level of the leads. Medtronic has developed a protocol under which MRI of the head region may be performed in patients with leads placed in the thoracic area. If abscess is found, prompt surgical removal of the leads and decompression of the abscess is indicated along with antibiotic coverage. Removal of the generator may also be appropriate with lead infection complication but this is variable. Epidural hematoma is a rare but potentially devastating complication of all epidural procedures. The introducer needle can lacerate epidural vessels and the passing of a lead out of the needle with subsequent manipulation of the lead during placement can traumatize vessels. Surgical paddle lead placement also has potential for vascular damage and bleeding. The incident of bleeding and subsequent hematoma formation would be expected to be greater in patients with delayed clotting. This complication would be expected to develop within hours of implant but may develop days later. Physical examination and CT or CT myelography most often lead to proper diagnosis. In evaluating patients with trial leads, removal of the trial leads and MRI is appropriate. Prompt neurosurgical decompression of the hematoma regions may significantly improve outcome. Lead Dislodgement Most commonly called lead migration is the displacement of a lead from its initial implant location. This complication occurs most often within the first 6 weeks after implant. Meticulous lead anchoring technique, lead location, and anchoring the lead with the lead under minimal stress will lessen the rate of lead dislodgement. Newer anchoring devices from the device companies will likely reduce the incidence of this complication. Movement of trial

Pain at the Pocket Site Chronic pain may develop within IPG pockets. Most often this pain is secondary to cutaneous nerve irritation at the outer margins of the pocket. Extending the pocket size 1 to 2 cm beyond the edge of the IPG dimensions during development of the pocket may reduce this unpleasant complication. Locating the IPG over bone may result in pressure pain over the periosteum. Over several months, a dense capsule surrounding the IPG may develop in some patients and become painful. Breaks in the insulation of leads or extension cables can cause a focal sharp burning pain when the stimulator is turned on.

Conclusion The efficacy of stimulating the dorsal spinal cord with epidurally placed electrodes is well documented in helping to control severe chronic pain from multiple sources. When appropriately applied in the overall management of selected pain conditions, long-term pain reduction and quality of life improvements can be realized. As clinical and laboratory research efforts continue along with device improvements, these devices are expected to become even more useful. As anchoring and other device technologies improve and physician surgical training and experience improve, overall complication rate is expected to diminish.

Intrathecal Pumps Implanted intrathecal drug infusion uses either an electric powered and programmable pump or a pressure infused delivery device. Both devices are connected to an implanted intrathecal catheter. The drug reservoir is contained within the pump and is periodically refilled by inserting a special non-coring needle through the skin into a port located within the middle portion of the pump body. Continuous intrathecal infusion of medications offers unique advantages in the management of severe spasticity as well as chronic severe malignant and nonmalignant pain.88-93 With intrathecal delivery, drugs are deposited within the CNS more directly to target receptors in the spinal cord and, to some extent, the brain. Intrathecal delivery bypasses gut or transdermal absorption limitations and first-pass drug metabolism. Because intrathecal delivery circumvents the blood brain barrier that affects

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the distribution of medications into the central nervous system, much smaller doses of medications are needed to afford the desired benefits. In addition, fewer cerebral and peripheral effects are generally experienced. These benefits come at the price of system complexity, risks, and required refills.

Indications and Patient Selection Implanted intrathecal drug infusion may be indicated for pain and spasticity with considerable overlap between the two groups. Spasticity arising from head and spinal cord injury, cerebral vascular accident, anoxic brain injury, drug or toxic CNS insults, or demyelinating conditions such as muscular sclerosis all have shown favorable response to intrathecal baclofen therapy. When spasticity is not well managed with oral medications or botulinum toxin injections, consideration may be given to implanted intrathecal baclofen infusion as a treatment adjunct. Most patients being considered for intrathecal drug infusion are being treated with other medications and therapies that have not been adequate or have led to undesirable side effects or complications. These patients are often challenging in their overall medical management and psychological and social needs. Patients suffering with chronic severe pain that is not well managed with oral or transdermal medications owing to medication side effects may also be offered an intrathecal drug trial and considered for system implantation if effective. Narcotic side effects tend to be less with continuous intrathecal administration compared to other methods of administration.94

Contraindication Contraindications for implantation are the following: known allergy to any of the infused drugs; systemic and local infections at the proposed implant location; cachectic and severely debilitated patient not having suitable body mass; those on anticoagulant medications that cannot be stopped for placement of the intrathecal catheter; those patients very near end of life; and patients not showing a suitable response to the intrathecal trial.

Pump Medications Currently the Food and Drug Administration (FDA) has approved morphine, baclofen, and ziconotide for intrathecal administration. These medications are commercially available in preservative-free formulations and are of sufficient concentration to be used alone or in combination. Many practitioners employ the services of an experienced compounding pharmacy to formulate mixtures of these and other medications that are not commercially available.95,96 Medications and mixtures not FDA approved are considered “off label” usage. Compounding pharmacies adhere to strict guidelines and test for sterility, tonicity, and pH, and they provide valuable feedback relating to the various medications being compounded. Considerations regarding drug concentrations, solubility, compatibility, and stability are important, and consultation with the compounding pharmacist is a necessity.97 Medications commonly used “off label” in intrathecal infusion include hydromorphone, clonidine, bupivacaine, fentanyl, and sufentanil. Other, less frequently utilize used “off label” medications include midazolam, meperidine, ropivacaine, neostigmine, adenosine, and ketorolac. Various drug combinations may be tried to provide optimal pain and spasticity control. Which drug or drugs to

Figure 41-21  Medtronic SynchroMed II 20 mL and 40 mL programmable infusion pumps. (Reprinted with the permission of Medtronic, Inc. ©2010.)

consider is often based on physician experience and the particular type of pain being managed. With the introduction of ziconotide, some treatment algorithms have changed. The reader is encouraged to research the literature and consult other physicians who are experienced in pump management when prescribing intrathecal mixtures.98,99-103

Types of Infusion Pumps Implanted intrathecal infusion pumps are of two general technologies: electronic programmable with a motor-driven roller pump; and nonprogrammable constant flow pumps. Constant flow pumps do not require a power source. They use a fixed orifice outlet from the reservoir which is held under a constant pressure by a collapsible compartment containing a gas/liquid mixture of Freon. As of this writing, two companies manufacture the majority of implanted infusion pumps: Medtronic and Johnson & Johnson. Medtronic currently manufactures only the SynchroMed II (Fig. 41-21). This device is programmable and uses a motor-driven roller pump. Johnson & Johnson’s device, the Codman 3000, is a constant flow pump and uses constant gas pressure from a liquid/gas mixture of Freon (Fig 41-22). The electronic programmable intrathecal infusion pumps manufactured by Medtronic (SynchroMed II) are the most commonly implanted infusion devices for pain and spasticity in the United States. Medtronic pumps are currently manufactured in 20 mL or 40 mL capacities with a catheter access port. Older generation programmable Medtronic pumps had 10 mL or 18 mL capacities with or without catheter access ports, and with or without suture loops. Medtronic also marketed a constant flow infusion pump (IsoMed) which is not currently in production. The IsoMed pump was available in 20, 35, and 60 mL volumes, with flow rates of 0.05, 1.0, and 1.5 mL/day. The IsoMed pump carries FDA approval for morphine sulfate infusion. Medtronic programmable infusion pumps (SynchroMed II) are FDA approved for morphine sulfate (Infumorph), baclofen (Lioresal Intrathecal) and ziconotide (Prialt). Johnson & Johnson’s Codman 3000 is FDA approved for morphine sulfate (Infumorph) and baclofen (Lioresal Intrathecal).

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Figure 41-22  Johnson & Johnson, Codman 3000 constant flow infusion pump with attached intrathecal catheter.

Intrathecal Catheters Several different catheters are or have been marketed by Medtronic. Current catheters are either a one-piece design with the same catheter dimensions the entire length or a two-piece design wherein the intrathecal or distal segment has a smaller outside dimension than the pump or proximal segment. These two segments are spliced together at the back incision region. Figure 41-23 shows the Medtronic two-piece catheter. Both Medtronic one- and two-piece catheters have the same internal diameter and a catheter volume of 0.0022 mL/cm of length. Both catheters have a radiopaque tip and six side holes near the tip. Each design has advantages and disadvantages and implanter preference generally dictates which is used. The Johnson & Johnson Codman offers the Flextip Plus catheter which is a 19 gauge one-piece design with a titanium-reinforced inner coil to resist kinking. Direct access to the catheter is occasionally useful in the management of intrathecal infusion devices. Generally with the ­SynchroMed II programmable pump, the port aids in the diagnosis of pump system failure and is accessed at a location near the catheter connector. Access to the catheter with the Codman constant flow pump is by way of a specially designed needle inserted through the access port. With the Codman pump, this port may be used for bolus administration, but with intrathecal placement it may also be aspirated. Bolus delivery using the SynchroMed II can be accomplished by programming, and bolus through the access port is generally not needed unless diagnostic testing is being undertaken. These catheter access ports are unfiltered and solutions are injected directly intrathecally. When accessing the catheter port, care is taken to avoid accidental overdose by injecting the contents of the catheter. A catheter may contain approximately 0.19 mL of solution. If, for example, the pump medication is baclofen 2000 mcg per mL, then there is 380 mcg of baclofen in the catheter (2000 micrograms times 0.19 mL). This, injected as a bolus, is often an overdose. Integral to all the implanted pumps is a submicron (.22 micron) bacterial filter. This filters the infused solution prior to entering the intrathecal catheter and reduces the risk of bacterial contaminated reservoir solutions being infused. The Codman 3000 constant flow pump has no batteries and can function for prolonged periods. SynchroMed II pumps generally function 4 to 8 years before battery depletion, depending on infusion rate. The battery is sealed within the pump and cannot be replaced. Changing the battery requires removal with replacement

Figure 41-23  Medtronic two-piece intrathecal catheter. (Reprinted with the permission of Medtronic, Inc. ©2010.)

of the pump. Near the end of battery life, the pump will indicate this condition when it is interrogated during refill. An audible tone from the pump can also be set to sound when the near end of battery life condition occurs. When end of battery life is indicated, it is advised to replace the pump prior to complete failure, which generally occurs within 4 weeks.

Preimplant Considerations A wide range of patients are considered for intrathecal drug delivery, including pediatric patients for intrathecal baclofen. Extremes of health are encountered in the malignant pain population, many times undergoing concurrent radiation and chemotherapy. Each group will have specific needs and considerations. Varied issues arise when dealing with these diverse patient groups. Close collaboration with managing neurologists, oncologists, internists, surgeons, and other health care providers and the patient’s support network is important for successful long-term outcomes. Careful discussion with the patient and care providers regarding the implant process, ongoing refill needs, and issues relating to catheter failure and other possible complications is required. Patients with ongoing infections, bleeding dyscrasia or prolonged bleeding secondary to antiplatelet medications or chemotherapy are closely evaluated.69,104 Body mass is important when considering pump size and pocket location.

Drug Trial Trialing intrathecal medications prior to system implant is useful and often required by payers. Baclofen is most often trialed as a single intrathecal dose of 50 to 100 mcg injected into the spinal fluid at the lower lumbar spine. If adequate benefit is not obtained with a

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41

Table 41-1  Comparing Ashworth and Modified Ashworth Scoring Ashworth Scale*

Modified Ashworth Scale†

0

No increase in tone

No increase in muscle tone

1

Slight increase in tone giving a catch when the limb is moved in flexion or extension

Slight increase in muscle tone, manifested by a catch and release or by minimal ­resistance at the end of the range of motion (ROM) when the affected part is moved in flexion or extension

1+

N/A

Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM

2

More marked increase in tone but limb is easily flexed

More marked increase in muscle tone through most of the ROM, but affected parts are easily moved

3

Considerable increase in tone, passive movement is difficult

Considerable increase in muscle tone, passive movement is difficult

4

Limb is rigid in flexion or extension

Affected part is rigid in flexion or extension

Score

*Ashworth, †Bohannon

1964. & Smith, 1987.

50 mcg dose, often a second trial of 100 mcg is considered. ­Ashworth or Modified Ashworth scoring of affected muscle groups is most often performed by experienced physical therapy practitioners prior to and at 30 minutes, 2, 4, and 6 hours after injection. This assists in documenting the patient’s response. The Ashworth Scale is a five-point scale (0, 1, 2, 3, or 4).105 Bohannon and Smith added a “grade 1+” to make a six-point scale and made minor changes to the definitions to increase the sensitivity. This is known as the Modified Ashworth Scale.106 Table 41-1 is a chart comparing the two Ashworth scales. A drop of at least two points is desired in either score. Other factors may also be assessed during this trial period such as frequency of spasms, increased range of motion, pain score, and changes in activities of daily living. Patients with lower extremity spasm may do worse with some ADLs such as pivot transfer where they depend on leg stiffness for support. These muscles often require long-term retraining if intrathecal baclofen infusion is instigated. A baclofen trial typically requires 6 to 8 hours to complete. Often, an initial phase of good benefit is followed by a period during which the baclofen effect is maximal and the patient is to “loose”. This is followed by another period of acceptable benefit as the baclofen effect begins to resolve and the patient returns to baseline tone. From the trial results, an estimate of a starting baclofen dose is made. However, intrathecal baclofen is most generally infused using programmable pumps, and dose adjustments are expected as the optimal dose is sought over the weeks and months after implant. Intrathecal drug trials of narcotics and other medications may be accomplished by single injections, sequential injections, or by placement of a catheter. An intrathecal or epidural catheter may be used and a continuous infusion of medications provided over several hours to days. The dose and mixture of medications may be adjusted during this period to assist in optimizing the desired effect. A wide range of patient responses may occur and can be delayed. Close observation of these patients is generally advised. Personnel experienced in managing spinal catheters and external spinal infusion pumps are important to reduce dosing errors and the incidence of catheter infections. Pain medication trials are subjective in that the amount of pain reduction is reported by the patient and cannot be measured. Significant placebo effect in these trials may occur and is difficult to control and factor. Most often the patient is observed for drug

reactions that may indicate the trialed drug is not appropriate. Some guidance as to the initial drug infusion rate can also be determined. When using a catheter, various mixtures of medications may be trialed rapidly and serve as a guide to the initial pump mixture.

Implant Process Implantation of an intrathecal pump and catheter is a surgical procedure requiring a surgical environment and techniques as described in the previous section on spinal cord stimulator implant.107,108 The pump is most generally implanted in the lower quadrant of the abdominal region, and the catheter is inserted in the lower lumbar region with the catheter tip advanced to an appropriate spinal level. Previous abdominal surgical procedure scarring or the presence of a suprapubic urinary catheter or gastrostomy feeding tubes will affect the planned pocket location. With the patient lying supine, the proposed pocket skin incision location is marked. In adults, typically a transverse incision slightly larger than the pump is made at the level of the lower portion of the umbilicus. Pumps and catheters may be implanted using general endotracheal anesthesia or local anesthesia with sedation. Communication with the patient is not required during implantation. Patients may report pain if the spinal cord or nerve roots are contacted during introducer placement or catheter manipulation. If there is increased concern for spinal cord or nerve damage, local anesthesia may be preferred so that the patient may report. Patients are placed in the lateral position padded and secured using straps and wide tape as needed. An axillary role is placed as customary for patents in this position. It is helpful to secure the patient in such a way as to not impede access to the lower spine and abdominal region. The proposed surgical areas are prepped using Betadine or chlorhexidine scrub followed by 3M™ DuraPrep, ­ChloroPrep, or other appropriate surgical prep. Complete draping of the surgical areas is required including the C-arm unit. Strict aseptic surgical technique is employed. C-arm fluoroscopy is required to verify spinal structures and level and to verify appropriate introducer placement and catheter tip location. Posteroanterior (PA) fluoroscopy imaging is initially used and the image is adjusted so that the intended insertion level is visualized in a true PA projection. The introducer is inserted below the level of the conus medullaris which is typically above

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Figure 41-24  Patient in left lateral position with the intrathecal introducer in place. The fluoroscopy unit is positioned to give a posteroanterior (PA) image.

L2 in adults. Figure 41-24 shows a patient in the left lateral position with the C-arm providing a PA view for placement of the intrathecal introducer. A slight paramedian introducer approach is used with as flat of an entry angle to the spine as is practical. The needle tip target is midline below the spinous process. When the introducer needle is inserted through the dura with the bevel aligned in the longitudinal axis, fewer dural fibers are cut. This may reduce the incidence of postdural puncture headache. The introducer is advanced using lateral radiographic imaging and is stopped midway in the spinal cannel. Figure 41-25 shows a lateral fluoroscopy image of the introducer and catheter projecting cephalad. The bevel position of the needle is indicated on the hub and after entry into the intrathecal space is rotated to point cephalad. Brief removal of the stylet will demonstrate copious CSF flow from the needle and is quickly replaced so as not to allow a large volume of CSF to escape. This is especially important in the pediatric patient where spinal CSF volume is minimal. The catheter tip is held near the needle hub and is inserted as soon as the stylet is removed. Gentle pressure only is required to pass the catheter and advancement is observed in the PA and lateral fluoroscopy projections until the radiopaque tip is at the intended spinal level. Occasionally as the catheter emerges from the introducer tip, it touches the anterior wall of the spinal canal. If this occurs, withdrawing the introducer slightly may allow the catheter to pass. Withdrawing a catheter from the introducer can result in sheering of the catheter. When a catheter fails to advance easily, remove the introducer and catheter together. The introducer can be reinserted at the same or different spinal level. A longitudinal incision is made against the needle and carried down to the fascia overlying the spinous processes. Blunt dissection is carried out to expose the site where the needle pierces the spinal fascia. A purse-string of nonabsorbable suture such as 0-silk is placed around the needle barrel incorporating the fascia. Figure 41-26 demonstrates a purse-string of 0-silk being placed around an introducer. The introducer is removed with the catheter stylet in place. After radiographic verification of the location of the catheter tip is made, the purse-string is tightened. When the stylet is removed, clear CSF should easily drip from the catheter. Occasionally, the CSF may require aspiration using a “Luer-Slip” tuberculin syringe at the pump connector end. A suitable anchor is slid onto the catheter and secured to the fascia with nonabsorbable suture as per manufacturer recommendations. When using a two-piece

Figure 41-25  Lateral fluoroscopy image of intrathecal introducer and catheter.

Figure 41-26  Purse-string of 0-silk placed around introducer.

catheter, the spinal segment is typically trimmed and a protective “boot” is slid onto the spinal segment. The spinal and pump segments are connected by a titanium pin from the thicker pump segment. Care is taken when making this connection because damage to the catheter may occur causing a hole and persistent CSF leakage with loss of benefit. Using a one-piece catheter does not generally require a splice at the spine but a pump connector is attached to the end of the catheter using nonabsorbable suture. A pocket is developed following incision of the skin at the previously marked site down to the subcutaneous fat layer. Blunt finger dissection and electrocautery is used in the subcutaneous fat tissue plane. The pocket is often placed toward midline and lower in the abdomen and pelvis. It is best to anchor pumps to the deep fascia, however, in very obese patients it may not be practical to place the pump against the abdominal fascia. In some circumstances, a pocket is developed within the subcutaneous fat layer. Pumps placed within a thick fat layer deep to the skin may be difficult to refill, are at increased risk of flipping or turning, and if

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Figure 41-28  Pump in pocket prior to skin closure.

Figure 41-27  Catheter passer may be bent to allow it to pass around the flank.

programmable, they may be hard to communicate with because of the distance. A hollow tunneling device is passed from the back incision to the pocket if using a two-piece catheter and from the pocket to the back incision when using a one-piece catheter. The tunneling device may be bent to conform somewhat to the intended path dimensions (Fig. 41-27) Alternately, the tunneling device may be passed to an intermediate incision located in the lower flank region using two separate passes. Nonabsorbable sutures are used to anchor the pump in the pocket. Three or four, typically 0-silk, are placed into the deep fascia and passed through corresponding suture loops. These sutures prevent the pump from rotating, flipping, and migrating laterally. The catheter connecter is secured to the pump as per manufacture recommendations. The catheter is coiled and held behind the pump and they are both gently placed into the pocket making sure the sutures do not directly touch the catheter. The ends of a pair of forceps may be placed into the loop of suture prior to tying several knots to create approximately 2 cm of slack. If these sutures are tied tightly, they tend to “saw” through the tissue with pump movements. Figure 41-28 shows a pump in the pocket ready for skin closure. A small coil of catheter is desired at the back incision to act as a strain relief. A small subcutaneous flap is developed to allow the catheter to coil in this region. Incisions are observed for bleeding and cauterized appropriately. Wounds are irrigated with antibiotic irrigation and closed in layers to reduce tension across the incision. An interrupted closure of buried knots using a minimally reactive suture such as polydioxanone (PDS) may reduce wound healing complications. This material also tends to provide a longer lasting approximation force than does polyglactin 910 (Vicryl). Skin staples, running nylon, Steri-Strips or tissue glue may also be employed. Gauze dressing is taped into place.

Postoperative Complications When wound healing complications arise at the back surgical site, there is concern with the increased opportunity for bacteria to enter the intrathecal space resulting in meningitis. Wound dehiscence may result secondary to persistent CSF leakage or seroma formation. In this situation, it may be reasonable to correct the defect and, in the uncontaminated wound, close the skin secondarily. However, if there is any indication of deep wound infection, the catheter and all components are removed; the infection is cleared, and after the area has healed, a catheter is again placed. Infected wounds where catheter components remain rarely heal by primary or secondary intention. Because of the significant increased risk of CNS infection, it is not appropriate to place an intrathecal catheter at the level of a dehisced wound until the wound is completely healed. Pump pocket wound healing complications are reduced by proper pocket creation, local flap development when needed, and closure with minimal stress at the incision. Even superficial infections may progress to involve deeper levels and the pocket. When infection of the pocket occurs, removal of the pump and catheter is warranted. An infection of the pump pocket can tract down the catheter path and involve the catheter implant site. Some reports of successful infection treatment “salvaging” the device have been given. These efforts are undertaken by experienced implant groups with knowledge of the risks and benefits of such attempts.107-111

Refilling the Pump Reservoir The computer within the Medtronic SynchroMed II calculates the expected pump volume based on the input volume at time of refill and the programmed infusion rate. The pump does not have a volume sensor. It will continue to infuse at the programmed rate until nearly empty. At a volume below 1.0 mL the infusion becomes gradually less and at a volume below approximately 0.6 mL, the infusion stops. There is a residual 1.4 mL within the pump that cannot be aspirated or pumped out. This residual drug

500  Spine

may be important when drug concentration changes are made and is the reason Medtronic advises that the reservoir be rinsed with the new drug prior to refill when a significant drug concentration change is made. The infusion will continue at the set rate until the reservoir is empty regardless of the calculated volume. The SynchroMed II has a refill port within the center of the pump and is accessed with a 22 gauge noncoring Huber needle and a catheter access port is located toward the outer edge near the pump catheter connector. The Medtronic refill port is designed for 500 accesses using the 22 gauge Huber needle. Huber needles lessen damage to the port with repeated entry. The catheter port is accessed with a 24 gauge non-coring Huber needle. Accidental injection of medication into the catheter access port and thus directly into the intrathecal space may have disastrous consequences. Therefore, the use of a standard refill “kit” containing the appropriate needles and guide template is recommended. The Johnson & Johnson, Codman 3000 will continue to infuse until the entire contents are depleted. Refill of the Codman pump is accomplished using a similar technique and again, use of the supplies available from the manufacturer is recommended. Access to the Codman catheter for bolus administration or aspiration of CSF is accomplished using a special needle also available from the manufacturer.

Refill Complications The installation of the medication into an intrathecal pump and associated programming of the programmable pumps is a major source of medical error. Most serious complications, including death, related to intrathecal drug infusion systems occur as a result of these errors. Intrathecal pumps often contain concentrated medications. If, at time of refill, the medication is accidentally injected into the pump pocket or surrounding tissues instead of the pump reservoir, serious complications may arise. When the medication is a concentrated narcotic, acute narcotic overdose will occur. Immediate supportive care should be instituted including airway management and ventilatory support as needed. Prolonged infusion of naloxone (Narcan) in an ICU may be necessary where long-term respiratory support and monitoring can be provided. A  prompt attempt may be made to aspirate the misplaced drug when practical. Accidental injection of baclofen into the pocket is of much less concern. Subcutaneously placed baclofen has minimal direct consequences except, when unrecognized; it will result in early termination of benefit. Other compounded medications accidentally placed into the pocket will have varying effects peculiar to the drug. If pump medications require compounding, concern is given as to the accuracy of the prescription and resultant compounded medication. It behooves the managing physician to understand the complexities of compounding intrathecal medications. Solubility limits, tonicity, pH, and incompatibilities of certain mixtures are considered. Intrathecal medications are prepared by compounding pharmacies using laminar flow hoods in a sterile environment practicing impeccable technique. Well trained and knowledgeable personnel with the utmost concern for accuracy, sterility, packaging, and validation of the product by appropriate testing using chemical assays, pH and tonicity measurement, and bacterial cultures will lessen complications. The managing physician is wise to know the details of this process and the people and processes involved to provide their patients optimal care.

Managing Patients with Intrathecal Infusion Pumps There is considerable variation among practices managing intrathecal drug infusion and the “art” of pump management is developed with experience. Long-term management of patients with intrathecal pumps containing narcotics is not simply to increase the dose. Continuous dose escalation of narcotics will lead to ­tolerance. A  “hyperalgesic” state may also develop when narcotic dosage is very high. As with any delivery route, chronic high-dose narcotic administration appears to inhibit the usual pain control mechanism.112-127a A few practitioners advocate using low doses of intrathecal morphine (less than 0.5 mg/day) to avoid some of the complications associated with dose escalation. Tolerance problems appear to be less with intrathecal baclofen and ziconotide.128,129 After attaining a stable infusion rate, dose escalation is not typically required to provide the same clinical efficacy. Infusion rates of these medications require only occasional adjustment when disease or health state changes are thought to be long term in nature.

Infusion System Failure Ongoing management of patients with intrathecal infusion systems by knowledgeable health care professionals is a valuable first source of information indicating there may be a malfunction. Between refills and especially at the time of refill, patients and patient care providers report or are questioned regarding symptoms and perceived benefits.130 If significant changes in benefit are reported, suspicion is raised and attention is given to the possibility of a system malfunction. Multiple factors will affect medication benefit and include patient illness, physical and psychological stress, medication changes, and disease progression or remission. Patient history and past issues at times of refills are also important. These are factored together with the physician’s personal knowledge of the patient to formulate an impression regarding how to proceed. Pump content volume discrepancy at time of refill may indicate a failure of the system to infuse the appropriate volume, indicating a catheter occlusion, or in rare situations, failure of the pump. Occasionally, lower than expected volume is found and may represent drug being diverted, internal failure of the pump, or most commonly, error at time of refill. When comparing expected pump volume and actual aspirated volume, several factors are considered. Syringe accuracy of ±5% is common. Syringe volume variance, along with differences in refill techniques, can produce significant variations when comparing actual with expected volumes. The expected pump volume is calculated by the internal computer of the programmable pumps and does not indicated actual volume. The volume expected in the Codman pump is calculated by multiplying the days of infusion by the pump infusion rate and subtracting this volume from the initial volume. Actual pump volume must be measured by aspiration of the entire reservoir contents at time of refill. This aspirated drug is discarded and not reused. When a patient suffers a profound reduction in benefit, there are several considerations. Symptom onset shortly after refill may indicate pump programming or drug errors. The refill event is reviewed, and if the pump is programmable, it is interrogated and the programming is confirmed. Instilled medication prescription is reviewed and if compounded medication was used, the compounding pharmacy is contracted to verify the prescription and the compounded medication that was supplied. Supportive care is

Spinal Cord Stimulation and Implanted Intrathecal Drug Infusion  501

instituted as indicated. This may include increased oral pain medication or oral baclofen. Patients will, on occasion, require hospitalization for parenteral antispasmodic or pain medications and on rare incidences, placement of a temporary intrathecal catheter to restart the intrathecal infusion.131 Often, prompt surgical correction of a catheter defect or replacement of a failed pump is best. Catheter Failure The ability to manage implanted intrathecal infusion pump and catheter system failure is important in the overall management of the patient. Most commonly, the spinal catheter fails and only in rare instances will the pump fail. Infused volume is small—as low as 0.3 mL/day in the Codman pumps and as low as 0.048 mL/day for the Medtronic SynchroMed II. Therefore, most generally, if a defect arises along the catheter, there is complete loss of benefit. Currently manufactured catheters are difficult to kink or occlude but are susceptible to cutting or punctures. Small defects or microfractures may prevent the medication from reliably reaching the intrathecal space. Meticulous implant technique, careful anchoring of the catheter to a deep fascial layer or ligament, appropriate pocket creation, and anchoring of the pump in the pocket will help reduce catheter damage. If the distal end of a catheter is in the intrathecal space and a defect manifests along some portion of that catheter, CSF leakage most often occurs with accumulation of CSF within the area of the defect. Diagnosing the nature and location of the failure may require significant effort and medical decision making. Plain AP and lateral radiographs of the pump and the entire catheter are useful to demonstrate if complete catheter fracture or dislodgement has occurred. Figure 41-29 shows a lateral radiograph whereon a catheter has pulled out of the intrathecal space and is coiled within the back implant region. This complication likely resulted from anchoring within the subcutaneous tissues and not at the spinal fascia. These radiographs cannot with certainty demonstrate catheter kinks or defects that do not cause complete catheter fracture. Catheter fracture and defects most often occur at the interspinal ligament, at connectors or anchor sites and within the pump pocket. If indicated, a medication bolus may be programmed using a programmable pump and the patient should be observed for improvement which would suggest the catheter is intact. The catheter access port may be accessed and CSF attempted to be aspirated. If CSF is easily aspirated, nonionic contrast suitable for intrathecal

Catheter coiled

administration may be injected and the flow of contrast followed and intrathecal spread confirmed. If CSF cannot be aspirated, contrast should not be injected because a bolus of medications contained within the spinal catheter segment is possible. If contrast spread is intrathecal, then reasonable assurance is made that the catheter is continuous, but this study cannot rule out the presence of small catheter defects. With small defects, the contrast can pass down the catheter into the intrathecal space without enough contrast passing out the defect to be easily detected. In this situation, an indium DTPA In 111 study may be useful to demonstrate the defect.132-134 This nuclear medicine study uses radioactive indium DTPA 111 (0.5 to 2 mCi) placed into the pump reservoir. The pump is allowed to infuse at its usual rate and the flow of indium is documented by serial scans over a period of time depending on the pump flow rate. The indium DTPA In 111 study can be accomplished without interrupting normal medication delivery or alternately the pump contents can be emptied and the indium DTPA In 111 can be added to saline placed into the pump. Indium DTPA In 111 will collect at a site where pump contents exit the catheter. Figure 41-30 demonstrates a small collection of indium DTPA In 111 at the spinal implant site and a large amount being infused into the spinal canal. This was a very small defect and was positional. With an intact catheter the indium DTPA tracer will be seen within the spinal canal. It is useful to place a lead blank or shield over the pump to reduce the tracer count the camera sees to improve the signal-to-noise ratio. In special situations, and using great care, a very small aliquot (less than 0.05 mL) of indium DTPA has been injected directly into the catheter access port and the pump has been allowed to run at its usual rate. In doing this, the tracer is only present in the catheter which considerably reduces the background noise and provides improved resolution. The risk of this technique is that when the catheter access port is injected, contents of the catheter are displaced. This can result in significant overdosing. This technique can be useful in those situations where the catheter dye study is apparently normal but a catheter failure is still of concern. After the dye study, the catheter is free of medication and a small aliquot of indium DTPA 111 can more safely be placed into the catheter. Indium DTPA 111 half-life is 2.83 days or 67.9 hours and is predominantly excreted in the urine. Rapid appearance of counts in the kidneys and the bladder is noted after the indium DTPA exits the catheter. Fluid accumulation at the spinal catheter insertion site or the pump pocket may indicate a CSF leak from a defect in the catheter. CSF pressure is transmitted down the catheter to the location of a defect. The flow rate from an intrathecal implanted pump is very small and if any defect along a catheter develops, CSF and pump

L ANT OBL

R POST OBL

Catheter tip out of spine SUPINE 20-Hour delay Figure 41-29  Catheter dislodgement from spine, which is coiled within the subcutaneous tissue.

Figure 41-30  Indium-111 DTPA collection at the spinal insertion site.

41

502  Spine

medications will flow out of the defect. This generally causes complete loss of benefit and often an accumulation of CSF at the site. CSF may track along the external surface of a catheter and accumulate at a distant site. Occasionally CSF leakage at the spinal insertion site or at a catheter splice or anchor in the back can track around the catheter tissue sheath and enter the pump pocket resulting in CSF collection. Other considerations for fluid collection would include seroma and infection. Generally, seroma and CSF accumulations are not associated with redness or skin temperature elevation. Early after implant, seroma accumulation is common and generally of little consequence. Aspiration of seroma fluid is avoided because the procedure has the potential of introducing bacteria into the area. If an infection is suspected, prompt aspiration of the fluid with appropriate Gram stain and culture will help direct antibiotic care. When a deep infection is diagnosed, prompt removal of the pump and catheter is advised. Eradication of an infection in the presence of implanted devices is very difficult and in the presence of an intrathecal catheter additional risks of CNS spread are ­imparted.107,108,111,135-137 If a fluid collection is suspected to contain CSF, a beta-2 transferrin assay can be useful. Beta-2 transferrin is a protein found almost exclusively in the CNS and spinal fluid.138 Persistent postural headache may arise as a result of CSF leakage around the catheter where it pierces the dura. This complication is reduced with the application of a purse-string suture placed around the introducer needle prior to its removal at time of implant.139 An x-ray-guided epidural blood patch may be helpful, understanding that this procedure carries some increased infection risk and the possibility of blood entering the intrathecal space.140-143 In persistent cases, surgical exploration of the implant area looking for possible catheter sources of the CSF leakage is recommended. This provides an opportunity to possibly witness CSF flow around the catheter where it enters the ligament or fascia. CSF leakage around the catheter may be accentuated by applying increased intrathoracic pressure by a Valsalva maneuver. On occasion, the solution is to remove the catheter, over-sew the area to close the site where the catheter pierced the ligament or fascia, and place another catheter. Catheter dislodgement can occur if the catheter is not properly anchored to deep fascia or as a result of a traumatic event. Also, if the pump is not anchored in the pocket and it rotates, over time the catheter can coil to the extent that it pulls the entire catheter into the pocket. If the catheter remains in the spinal implant region, the back incision may be opened and that portion of catheter, along with the anchor and splices if any, is removed and a new spinal segment is implanted and spliced to the remaining pump segment. If the catheter has pulled back into the pump pocket, then the pocket is opened along with the back site with placement of a new catheter and tunneling. When catheters fracture at the interspinal ligament, most often the fragment will migrate into the intrathecal space. Unless the fragment causes some neurologic sequela, it most frequently is left in the intrathecal space and attempts to retrieve it are not made. Antibiotic effectiveness may be reduced in CNS infections when retained fragments are present.144,145

Catheter Tip Inflammatory Mass Patients presenting with relatively sudden or unexplained decreased therapeutic response, pain, neurologic changes such as weakness and reflex changes should be evaluated for the presence of a mass at the catheter tip.146 These masses are not well understood but appear to be associated more with the infusion of highly concentrated

narcotic preparations. The incidence is expected to be greater than 0.5% of all intrathecal catheters and has been reported with morphine and, to a lesser degree, with baclofen.147-151 Catheter granulomatous or inflammatory masses appear to develop over time and may compress the spinal cord. Diagnosis is best made using a highresolution MRI scanner. Gadolinium contrast may demonstrate enhancement of the mass, suggesting its inflammatory nature. Where MRI is contraindicated or not available, CT myelography of the catheter tip region may be useful. Plain radiograph examination prior to MRI or CT is used to direct the scans to the area of most interest near the catheter tip. Scanning two spinal levels above and three levels below the catheter tip usually is sufficient. The proper management of a catheter tip mass, although debated generally, includes neurosurgical consultation. Cord compression resulting in significant neurologic compromise typically is treated by prompt neurosurgical removal of the intrathecal mass along with the catheter. When neurologic symptoms allow, pulling back the catheter to a location below the mass and changing the pump drug mixture may be enough to allow resolution.

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504  Spine   55. de Vos CC, Rajan V, Steenbergen W, et al. Effect and safety of spinal cord stimulation for treatment of chronic pain caused by diabetic neuropathy. J Diabetes Complications. 2009;23(1):40-45.   56. Kumar K, Toth C, Nath RK. Spinal cord stimulation for chronic pain in peripheral neuropathy. Surg Neurol. 1996;46(4):363-369.   57. Francaviglia N, Silvestro C, Maiello M, et al. Spinal cord stimulation for the treatment of progressive systemic sclerosis and Raynaud’s syndrome. Br J Neurosurg. 1994;8(5):567-571.   58. Raso AM. [Results of electrostimulation of the spinal cord in Raynaud’s disease and syndrome]. J Mal Vasc. 1989;14(1):52-54.   59. Kothari S. Neuromodulatory approaches to chronic pelvic pain and coccygodynia. Acta Neurochir Suppl. 2007;97:365-371.   60. Kapural L, Narouze SN, Janicki TI, Mekhail N. Spinal cord stimulation is an effective treatment for the chronic intractable visceral pelvic pain. Pain Med. 2006;7(5):440-443.   61. Deer TR. Current and future trends in spinal cord stimulation for chronic pain. Curr Pain Headache Rep. 2001;5:503-509.   62. Kapural L, Deer T, Yakovlev A, et al. Technical aspects of spinal cord stimulation for managing chronic visceral abdominal pain: the results from the national survey. Pain Med. 2010;11:685-691.   63. Deer TR. Current and future trends in spinal cord stimulation for chronic pain. Curr Pain Headache Rep. 2001;5(6):503-509.   64. Pinter MM, Gerstenbrand F, Dimitrijevic MR. Epidural electrical stimulation of posterior structures of the human lumbosacral cord: 3. Control of spasticity. Spinal Cord. 2000;38(9):524-531.   65. Cioni B, Meglio M, Prezioso A, et al. Spinal cord stimulation (SCS) in spastic hemiparesis. Pacing Clin Electrophysiol. 1989;12:739-742.   66. Maiman DJ, Mykleburst JB, Barolat-Romana G. Spinal cord stimulation for amelioration of spasticity: experimental results. Neurosurgery. 1987;21(3):331-333.   67. Koulousakis A, Buchhaas U, Nittner K. Application of SCS for movement disorders and spasticity. Acta Neurochir Suppl. 1987;39: 112-116.   68. Dimitrijevic MM, Dimitrijevic MR, Illis LS, et al. Spinal cord stimulation for the control of spasticity in patients with chronic spinal cord injury: I. Clinical observations. Cent Nerv Syst Trauma. 1986;3(2):129-144.   69. Horlocker TT, Wedel DJ, Rowlingson JC, et al. Regional anesthesia in the patient receiving antithrombotic or thrombolytic therapy: American Society of Regional Anesthesia and Pain Medicine Evidence-Based Guidelines (Third Edition). Reg Anesth Pain Med. 2010;35(1):64-101.   70. Lai HY, Lee CY, Lee ST. High cervical spinal cord stimulation after failed dorsal root entry zone surgery for brachial plexus avulsion pain. Surg Neurol. 2009;72(3):286-289.   71. Kreis PG, Fishman SM. Spinal Cord Stimulation: Percutaneous Implantation Techniques. New York: Oxford University Press; 2009.   72. Foletti A, Durrer A, Buchser E. Neurostimulation technology for the treatment of chronic pain: a focus on spinal cord stimulation. Expert Rev Med Devices. 2007;4(2):201-214.   73. Oakley JC, Prager JP. Spinal cord stimulation: mechanisms of action. Spine. 2002;27(22):2574-2583.   74. Krames E. Spinal cord stimulation: Indications, Mechanism of Action, and Efficacy. Curr Rev Pain. 1999;3(6):419-426.   75. Maruyama Y, Shimoji K. [Epidural spinal cord stimulation: its efficacy and mechanisms]. Gan No Rinsho. 1985;31(suppl 6):729-735.   76. Kumar K, Wilson JR. Factors affecting spinal cord stimulation outcome in chronic benign pain with suggestions to improve success rate. Acta Neurochir Suppl. 2007;97:91-99.   77. Doleys DM. Psychological factors in spinal cord stimulation therapy: brief review and discussion. Neurosurg Focus. 2006;21(6):E1.   78. Beltrutti D, Lamberto A, Barolat G, et al. The psychological assessment of candidates for spinal cord stimulation for chronic pain management. Pain Pract. 2004;4(3):204-221.   79. Horlocker TT, Wedel DJ, Rowlingson JC, et al. Regional anesthesia in the patient receiving antithrombotic or thrombolytic therapy: American Society of Regional Anesthesia and Pain Medicine Evidence-Based Guidelines (Third Edition). Reg Anesth Pain Med. 2010;35(1):64-101.

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Spinal Cord Stimulation and Implanted Intrathecal Drug Infusion  505 102. Hassenbusch SJ, Portenoy RK, Cousins M, et al. Polyanalgesic Consensus Conference 2003: an update on the management of pain by intraspinal drug delivery—report of an expert panel. J Pain Symptom Manage. 2004;27(6):540-563. 103. Mironer YE. Re: polyanalgesic survey and consensus report. J Pain Symptom Manage. 2001;21(4):269-272. 104. Horlocker TT, Wedel DJ, Benzon H, et al. Regional anesthesia in the anticoagulated patient: defining the risks (the second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med. 2003;28(3):172-197. 105. Ashworth B. Preliminary trial of carisoprodol in multiple sclerosis. Practitioner. 1964;192:540-542. 106. Bohannon RW, Smith MB. Interrater reliability of a modified Ashworth scale of muscle spasticity. Phys Ther. 1987;67(2):206-207. 107. Albright AL, Turner M, Pattisapu JV. Best-practice surgical techniques for intrathecal baclofen therapy. J Neurosurg. 2006;104(suppl 4): 233-239. 108. Vender JR, Hester S, Waller JL, et al. Identification and management of intrathecal baclofen pump complications: a comparison of pediatric and adult patients. J Neurosurg. 2006;104(suppl 1):9-15. 109. Borowski A, Littleton AG, Borkhuu B, et al. Complications of intrathecal baclofen pump therapy in pediatric patients. J Pediatr Orthop. 2010;30(1):76-81. 110. Fjelstad AB, Hommelstad J, Sorteberg A. Infections related to intrathecal baclofen therapy in children and adults: frequency and risk factors. J Neurosurg Pediatr. 2009;4(5):487-493. 111. Atiyeh BS, Hayek SN, Skaf GS, et al. Baclofen pump pocket infection: a case report of successful salvage with muscle flap. Int Wound J. 2006;3(1):23-28. 112. Ghafoor VL, Epshteyn M, Carlson GH, et al. Intrathecal drug therapy for long-term pain management. Am J Health Syst Pharm. 2007;64(23):2447-2461. 113. Noble M, Treadwell JR, Tregear SJ, et al. Long-term opioid management for chronic noncancer pain. Cochrane Database Syst Rev. 2010(1):CD006605. 114. Hay JL, White JM, Bochner F, et al. Hyperalgesia in opioid-managed chronic pain and opioid-dependent patients. J Pain. 2009;10(3): 316-322. 115. Hines S, Theodorou S, Williamson A, et al. Management of acute pain in methadone maintenance therapy in-patients. Drug Alcohol Rev. 2008;27(5):519-523. 116. Filitz J, Ihmsen H, Gunther W, et al. Supra-additive effects of tramadol and acetaminophen in a human pain model. Pain. 2008;136(3): 262-270. 117. Koppert W, Schmelz M. The impact of opioid-induced hyperalgesia for postoperative pain. Best Pract Res Clin Anaesthesiol. 2007;21(1): 65-83. 118. Imai S, Narita M, Hashimoto S, et al. Differences in tolerance to anti-hyperalgesic effects between chronic treatment with morphine and fentanyl under a state of pain. Nihon Shinkei Seishin Yakurigaku Zasshi. 2006;26(5-6):183-192. 119. Athanasos P, Smith CS, White JM, et al. Methadone maintenance patients are cross-tolerant to the antinociceptive effects of very high plasma morphine concentrations. Pain. 2006;120(3):267-275. 120. Chu LF, Clark DJ, Angst MS. Opioid tolerance and hyperalgesia in chronic pain patients after one month of oral morphine therapy: a preliminary prospective study. J Pain. 2006;7(1):43-48. 121. Koppert W. [Opioid-induced analgesia and hyperalgesia]. Schmerz. 2005;19:386-394. 122. Mao J, Sung B, Ji RR, Lim G. Chronic morphine induces downregulation of spinal glutamate transporters: implications in morphine tolerance and abnormal pain sensitivity. J Neurosci. 2002;22(18):8312-8323. 123. Streltzer J. Pain management in the opioid-dependent patient. Curr Psychiatry Rep. 2001;3(6):489-496. 124. Compton P, Charuvastra VC, Ling W. Pain intolerance in opioidmaintained former opiate addicts: effect of long-acting maintenance agent. Drug Alcohol Depend. 2001;63(2):139-146.

125. Doverty M, White JM, Somogyi AA, et al. Hyperalgesic responses in methadone maintenance patients. Pain. 2001;90(1-2):91-96. 126. Herrero JF, Laird JM, López-Garcia JA. Wind-up of spinal cord neurones and pain sensation: much ado about something? Prog Neurobiol. 2000;61(2):169-203. 127. Crain SM, Shen KF. Opioids can evoke direct receptor-mediated excitatory effects on sensory neurons. Trends Pharmacol Sci. 1990;11(2): 77-81. 127a. Lee M, Silverman SM, Hansen H, Patel VB, Manchikanti L. A comprehensive review of opioid-induced hyperalgesia. Pain Physician. 2011;14(2):145-161. 128. Heetla HW, Staal MJ, Kliphuis C, van Laar T. The incidence and management of tolerance in intrathecal baclofen therapy. Spinal Cord. 2009;47(10):751-756. 129. McGivern JG. Ziconotide: a review of its pharmacology and use in the treatment of pain. Neuropsychiatr Dis Treat. 2007;3(1):69-85. 130. Rawlins PK. Intrathecal baclofen therapy over 10 years. J Neurosci Nurs. 2004;36(6):322-327. 131. Bellinger A, Siriwetchadarak R, Rosenquist R, Greenlee JD. Prevention of intrathecal baclofen withdrawal syndrome: successful use of a temporary intrathecal catheter. Reg Anesth Pain Med. 2009;34(6): 600-602. 132. Rosenson AS. Indium-111 DTPA flow study to evaluate surgically implanted drug pump delivery system. Clin Nuclear Med. 1990;15(3):154-156. 133. Hoving MA, Smulders NM, Abdul Fatah B, et al. The use of an indium111 DTPA flow study in the evaluation of a lumbar swelling in a girl with a baclofen pump. Neuropediatrics. 2006;37(2):99-101. 134. Schmidt E, Oates E. In-111 DTPA to evaluate the patency of an implanted intrathecal infusion pump. Clin Nucl Med. 1997;22(11):768-770. 135. Borowski A, Shah SA, Littleton AG, et al. Baclofen pump implantation and spinal fusion in children: techniques and complications. Spine. 2008;33(18):1995-2000. 136. Kallweit U, Harzheim M, Marklein G, et al. Successful treatment of methicillin-resistant Staphylococcus aureus meningitis using linezolid without removal of intrathecal infusion pump. Case report. J Neurosurg. 2007;107(3):651-653. 137. Douglas AF, Weiner HL, Schwartz DR. Prolonged intrathecal baclofen withdrawal syndrome. Case report and discussion of current therapeutic management. J Neurosurg. 2005;102(6):1133-1136. 138. Skedros DG, Cass SP, Hirsch BE, Kelly RH. Beta-2 transferrin assay in clinical management of cerebral spinal fluid and perilymphatic fluid leaks. J Otolaryngol. 1993;22(5):341-344. 139. Singh PK, Jain R, Mishra S, et al. Management of pericatheter cerebrospinal fluid leak after intrathecal implantation of a drug delivery system. Am J Hosp Palliat Care. 2008;25(3):237-239. 140. Singh PK, Jain R, Mishra S, et al. Management of pericatheter cerebrospinal fluid leak after intrathecal implantation of a drug delivery system. Am J Hosp Palliat Care. 2008;25(3):237-239. 141. Liao YJ, Dillon WP, Chin CT, et al. Intracranial hypotension caused by leakage of cerebrospinal fluid from the thecal sac after lumboperitoneal shunt placement. Case report. J Neurosurg. 2007;107(1): 173-177. 142. Huch K, Kunz U, Kluger P, Puhl W. Epidural blood patch under fluoroscopic control: non-surgical treatment of lumbar cerebrospinal fluid fistula following implantation of an intrathecal pump system. Spinal Cord. 1999;37(9):648-652. 143. Kumar V, Maves T, Barcellos W. Epidural blood patch for treatment of subarachnoid fistula in children. Anaesthesia. 1991;46(2):117-118. 144. Medtronic. Medtronic: Syncromed, Isomed: Implantable Infusion Systems, Information for Prescribers. 1–34. 2009. Medtronic. 145. Forsythe A, Gupta A, Cohen SP. Retained intrathecal catheter fragment after spinal drain insertion. Reg Anesth Pain Med. 2009;34(4):375-378. 146. Medtronic, George Aram. Updated Information—Inflammatory mass (granuloma) at or near the distal tip of intrathecal catheters. 1–8. 2008. Medtronic.

41

506  Spine 147. Deer TR, Raso LJ, Coffey RJ, Allen JW. Intrathecal baclofen and catheter tip inflammatory mass lesions (granulomas): a reevaluation of case reports and imaging findings in light of experimental, clinicopathological, and radiological evidence. Pain Med. 2008;9(4):391-395. 148. Hassenbusch S, Burchiel K, Coffey RJ, et al. Management of intrathecal catheter-tip inflammatory masses: a consensus statement. Pain Med. 2002;3(4):313-323. 149. Coffey RJ, Burchiel K. Inflammatory mass lesions associated with intrathecal drug infusion catheters: report and observations on 41 patients. Neurosurgery. 2002;50(1):78-86.

150. Murphy PM, Skouvaklis DE, Amadeo RJ, et al. Intrathecal catheter granuloma associated with isolated baclofen infusion. Anesth Analg. 2006;102(3):848-852. 151. Deer TR. A prospective analysis of intrathecal granuloma in chronic pain patients: a review of the literature and report of a surveillance study. Pain Physician. 2004;7(2):225-228.

Sympathetic Neural Blockade

42

Jeffrey D. Petersohn, MD

The sympathetic nervous system contains some of the afferent and efferent neural pathways necessary for generation, perpetuation, or treatment of certain clinical pain states. Sympathetic neural block­ ade may be useful in differentiating neuropathic pain processes that involve the sympathetic nervous system (sympathetically main­ tained/mediated pain—SMP) from those that do not (sympathetic­ ally independent pain—SIP). Most, but not all, SMP fulfills the clinical criteria for complex regional pain syndrome (CRPS) type 1 or type 2.1 The precise pathophysiology of SMP/CRPS is not fully under­ stood, but loss of tonic sensory neuronal input associated with peripheral or other nerve injury produces chronically disordered information processing in the dorsolateral spinal cord with sub­ sequently inappropriate responses to afferent sensory input and increased efferent sympathetic outflow.2-4 Typically, patients report severe burning discomfort or pain, or abnormal sensations, that may occur either spontaneously or secondary to even low-thresh­ old stimuli. Physical findings, consistent with altered sympathetic tone, include erythema, edema, altered skin temperature, discol­ oration, and dystrophic changes of the skin, nails, and underlying bone and joints.2-5 Patients often exhibit guarding behaviors and physical findings consistent with disuse atrophy. Other pain processes, such as visceral pain processes, may involve sympathetic afferents but may not produce a typical clini­ cal composite of CRPS. Sympathetic nervous system involvement in visceral pain might be manifested as cutaneous hyperalgesia. Pain involving the sympathetic nervous system is accompanied by changes in central pain processing at spinal cord and higher levels. Functional magnetic resonance imaging (MRI) demonstrates changes in cere­ bral blood flow at thalamic and cortical levels in CRPS as well as in other chronic pain states,6,7 but the precise anatomic loci and molec­ ular pharmacology of the sympathetic nervous system involvement remain ill-defined and generalized; changes are not limited to the painful side of the brain if the initial injury is unilateral.8 SMP is challenging to treat and it may be that earlier inter­ vention increases the likelihood of successful treatment. The con­ dition may be suspected when common limb disorders have been excluded and/or complaints of pain far exceed the nominal injury with or without signs or symptoms suggestive of altered sympa­ thetic tone. SMP is a clinical diagnosis which may be supported by the presence of characteristic findings on physical examination, plain radiographs, triple-phase bone scan, thermogram, or sig­ nificant pain relief with sympathetic blockade.2,4,5,9-11 MRI is often helpful in differentiating subacute or chronic nondisplaced frac­ tures, pseudarthrosis, or neuroma, which are amenable to prompt

surgical treatment, but manifest with a similar clinical constellation. Aggressive treatment protocols are required to obtain successful lasting pain relief and prevent chronic dystrophic changes. Local or regional sympathetic blockade is the cornerstone of treatment for SMP and is thought to help by interrupting and disorganizing the inappropriate sympathetic activity.3,4 Multimodal treatments appear to offer improved prospects for clinical success.12 Guanethidine, bretylium, or reserpine by intravenous or intra­ venous regional technique are not efficacious. Local anesthetics or analogs administered by oral, subcutaneous, intravenous, or intravenous regional techniques have also failed to demonstrate efficacy. These results may reflect the complexity of the underly­ ing pathophysiology including, but not limited to, phenotypic shift of Aβ fibers to express substance P receptors, proliferation of ectop­ic α-adrenergic receptors, alterations in Na+ channel recep­ tors or responsiveness to TNF-α which may accompany pathologic states. Changes noted in biologic markers, such as DRG calcitoningene-related peptide (CGRP) seen with neural blockade, do not correlate with treatment outcome. Specific effects of sympathetic neural blockade on receptors for glutamine, NMDA, TRK, other vanilloids, or substance P are not known. Although physical therapy may be beneficial for analgesic modalities, for reduction of edema, and for promotion of active mobilization and reconditioning of involved extremities, common psychological comorbid conditions include anxiety, depression, and emergence of clinical personality disorders, similar to those seen in other patients with chronic pain. Recalcitrant CRPS unresponsive to traditional techniques may respond to spinal cord stimulation.13 Surgical sympathectomy may be considered for refractory circumstances, but success is far from assured and the duration of improvement is variable. Classic targets for sympatholysis are the stellate ganglion for facial and upper extremity pain, the celiac plexus for abdominal pain, the superior hypogastric plexus for pelvic pain, the lumbar sympathetic chain for lower extremity pain, and the ganglion impar for perineal pain. In addition, the thoracic sympathetic ganglia can be blocked for the treatment of hyperhidrosis or for pain of pleural or esophageal origin. It is the purpose of this chapter to describe some of the most commonly employed techniques for sympathetic nerve block, including indications, techniques, complications, and where con­ sensus exists, outcomes and recommendations for use. In the past decade, the putative role of the sympathetic ner­ vous system in clinical pain has become more subtle and more com­ plex with emerging neuroanatomic evidence for dual sympathetic and somatic innervation of many structures including cervical and 507

508  Spine

lumbar zygapophysial joint capsules. Curiously, however, painful zygapophysial spinal joints can be successfully treated with thermal radiofrequency neurolysis (of the medial branches) and the author is unaware of any proven case of zygapophysial joint pain resolved by sympathetic neural blockade. RF lesioning of the medial branch does not, when properly conducted, produce CRPS.14,15 The role of dual sympathetic and somatic innervation of the lumbar interver­ tebral disc has provided a putative basis for treatment of discogenic pain by sympathetic neural blockade or by RF lesioning of the gray rami communicantes by RF thermolysis.16 Sympathetic nerve block is often used in a diagnostic capacity for interruption of afferent or efferent neural pathways. Results of neural blockade generally, but do not always, correlate with out­ comes from repetitive neural blockade, surgical sympathectomy, and percutaneous chemical, cryotherapeutic, or thermolytic (RF lesioning) procedures. Limb or visceral pain, and in particular CRPS, which responds only transiently to sympathetic block may be improved with spinal cord stimulation.17 Clinical series and trials provide statistical evidence support­ ing circumscribed use of sympathetic nerve blocks, but a Cochrane review recommends that these techniques require thoughtful con­ sideration for incorporation into clinical practice as well as addi­ tional research. Much of the literature is confounded by issues of adequate epidemiologic case definition and, in many circumstances, the use of sympathetic nerve blocks to affirm an etiologic diagnosis may be a troublesome affirmation of the use of circular logic. The specialty of interventional pain practice remains in active technologic transition with some practitioners continuing to per­ form sympathetic nerve block interventions without fluoroscopy, many routinely employing fluoroscopic or computed tomography (CT) guidance, and others adopting ultrasound-guided techniques. As in many areas of medicine, new knowledge and technology pro­ vide opportunities to verify and improve existing protocols for diag­ nosis and treatment of sympathetically mediated pain, as well as a responsibility to discard ineffective interventions. Unfortunately, economic pressures for rapid and highly successful treatments will inappropriately target procedures used for the diagnosis and treat­ ment of obscure or ill-defined pain processes, including pain that may originate with or involve the sympathetic nervous system. Research into SMP is challenging to interpret as physicians incorporate emerging knowledge, moving from the diagnosis of clinical syndromes of SMP by varied panoply of symptoms and findings to conditions with neuro-bioanatomically defined mech­ anisms. The practicing clinician is challenged when consulting experts or the literature because much of the literature on sym­ pathetic nerve blocks is historically composed of case series. The limited number of patients with specific conditions who can be studied and the protean clinical presentations seen by individual practitioners or groups makes consistent evidence-based reviews or meta-analysis difficult and confounds efforts to delineate opti­ mal treatment approaches. Literature often incorporates broad epidemiologic case definitions, which may not accurately reflect the underlying biologic basis for pain. Older studies use patients who might presently be excluded by imaging studies and diagnostic blocks, but whose conditions were diagnosed at the time of origi­ nal literature publication with state-of-the-art care. Although truly efficacious procedures may exist for sympathetic pain, the limited effect size and number needed to treat analysis (NNT) often sug­ gests clinical restraint and, frustratingly, further research. In some situations, use of targets anatomically adjacent to sympathetic nerve structures, but without image guidance, may

suggest clinical efficacy,18 but more highly directed treatments may not be supportive.19 Substantial literature is devoted to case reports of complications of interventional treatment for sympathetic pain, including inadver­ tent intravascular injection of local anesthetic, pneumothorax, inad­ vertent nerve root or plexus injection, subarachnoid injection, or neural injury—many of which may be reducible by use of intermit­ tent multiplanar image-guided technique during needle placement. Inadvertent injection into adjacent neural or vascular structures can usually be detected by careful injection of radio-opaque contrast agents under continuous fluoroscopy with typical and suboptimal patterns of contrast for each procedure described in a number of textbooks and manuals. Expectable complications will continue to occur due to the physiologic effects of neural blockade, such as limb warmth, Horner syndrome, and hypotension. Practitioners must remain vigilant for such effects, especially when patients are taking an adrenergic antagonist medication, such as a beta blocker. Intra­ venous access and sufficient patient monitoring must be available within the facilities where such procedure are performed so that these problems can be safely managed. Unfortunately, complica­ tions resulting from pathologic or ill-described human anatomy or bleeding from needle passage through highly vascular tissue may be reduced by diligent technique, but not eliminated completely. Sympathetic neural blockade should be performed with appro­ priate imaging guidance (fluoroscopy, ultrasound, CT, MRI) and practitioners should be generally knowledgeable regarding regional anatomy and potential complications. These procedures should only be conducted by physicians where adequate facilities are available for patient safety, including physiologic monitoring and imaging, and where resuscitative measures may be implemented expeditiously, if needed. Intravenous access should be established preoperatively when hypotension or bradycardia are reason­ ably likely so that expeditious management can ensue. Absolute or relative contraindications to procedural interventions must be respected or when reasonably possible, mitigated by medical means preoperatively, consistent with generally held standards for inter­ ventional pain practice, including, but not limited to the following: Pregnancy Local or systemic infection ll Coagulopathy, anticoagulant or antiplatelet agent use ll Coexisting medical or surgical disease including immunocom­ promised states ll Challenging anatomic circumstances (tumor, deformity, postsur­ gical changes including prosthetic vascular device placement) ll Morbid obesity, severe osteopenia, or deformity that limits imaging ll Moving, unwilling, or uncooperative patient ll ll

Patients should be counseled preoperatively regarding the anticipated procedure, likely outcomes, expectable complications, and risks. The practitioner should be aware of the relevant laws (state, province, or country) regarding the essence and nature of this required discussion and standards for documentation, includ­ ing written consent. This chapter is not intended to be comprehen­ sive in scope and is not intended as a substitute for formal training and supervised experience in the performance of the procedures discussed. This chapter will discuss the following techniques: Sphenopalatine (pterygopalatine) ganglion block Stellate ganglion block ll Celiac plexus block ll ll

Sympathetic Neural Blockade  509

Celiac plexus and splanchnic nerve block Lumbar sympathetic nerve block ll Hypogastric plexus block ll Ganglion impar block ll ll

General Considerations for Sympathetic Neural Blockade Preoperative evaluation with CT, MRI, or ultrasound imaging is not regularly required for sympathetic nerve blocks; however this may be considered when planning optimal approaches for patients with specific disease states, prior surgery, or deformity which may affect safe or efficient access to the planned anatomic target or where ana­ tomic distortion of the target anatomy is anticipated. Supplemental oxygen, intravenous access, and physiologic monitoring including ECG, oxygen saturation, and blood pressure is typically required. The patient should be maintained nothing by mouth (NPO) prior to all sympathetic blocks, consistent with usual standards for major regional nerve block, typically 4 hours mini­ mum for clear liquids and 6 to 8 hours for solid foods. Apprehen­ sive patients may benefit from oral or intravenous sedation, given solely at the discretion of the treating physician, if there are no other medical contraindications. All techniques require antiseptic skin preparation and most operators prefer use of sterile paper or cloth drapes. The operator customarily wears sterile gloves and follows aseptic technique. Commonly used anesthetic agents include lidocaine 1%, or bupivacaine in 0.125%, or 0.25% concentrations. Choice of a specific local anesthetic agent or concentration is based on physician pref­ erence and experience because the literature analysis is confounded by wide variations in injectate volume, variable use of imaging guidance, and variable outcome criteria are used. Local anesthetics should be pyrogen and preservative free. No vasoconstrictor, such as epinephrine or phenylephrine, should be used. Second-generation, low osmolality radiologic contrast agents often used to verify ana­ tomic distribution of injectate include iohexol or iopamidol in 240 to 300 mOsm concentration. A third-generation contrast agent or gadolinium, more commonly used for MRI imaging, may be con­ sidered in patients with documented allergy to second-generation agents. Compromised renal function is a contraindication to the use of gadolinium. Although digital subtraction angiography (DSA) may be more sensitive than continuous fluoroscopy in demonstrating inadver­ tent arterial injection, DSA has not yet been widely adopted to rep­ resent a standard of care. Local distribution of injected contrast, either outlining the tar­ geted neural structure or filling of the surrounding anatomic osseomusculo-fascial compartment without vascular runoff should be observed on live fluoroscopy and confirmed in at least two fluoro­ scopic planes. Biplanar fluoroscopic images should be retained for documentation of technical adequacy of the procedure. Evidence for vascular injection, seen as a “flash” of contrast on fluoroscopy or by visible pulsations of a rapidly running off of contrast agent, requires withdrawal of the needle and reassessment of the anatomy before further injection attempts are made. Assessment of the visual analog scale (VAS) pain scores and function of the painful extremity or structure should be docu­ mented pre- and postoperatively. Documentation should also record any complications or side effects, as well as the ultimate

duration of improvement that follows each procedure. Often optimal physical therapy can be undertaken immediately fol­ lowing recovery from sedation—during the period of most potent analgesia from the neural blockade. Careful coordination between interventionalists and physical therapy departments will optimize care.

Stellate Ganglion Block (SGB) Anatomy The stellate ganglion is formed by the fusion of the inferior cervical and superior thoracic sympathetic ganglia and provides most of the sympathetic innervation to the head, neck, upper extremity, and a portion of the upper thorax. The ganglion is typically about 2.5 cm in length and is located at the root of the C7 transverse process; it lies anterolateral to the longus colli muscle. The ganglion is anterior to the transverse pro­ cess in the sagittal plane and posterior to the apical pleura which rises above the level of the first rib, posing a hazard of pneu­ mothorax for anterior approaches at the C7 level or below. The carotid artery is anterior to the ganglion and the vertebral artery is anterolateral inferiorly, subsequently crossing over the sympathetic chain as it ascends to enter the foramen transversarium at C6 or above in 95% of individuals.20,21 At C6, the inferior thyroid artery is also anterior to the ganglion. Sympathetic nerve branches from the stellate ganglion extend to the brachial plexus, subclavian and vertebral arteries as well as the brachiocephalic trunk.22 Cardiac sympathetic nerves arise from the ganglion as does the vertebral nerve, which provides sympathetic innervation of the fibrous cap­ sules of the zygapophysial and intervertebral joints and meningeal structures.15 Merged inferior cervical and thoracic ganglia are present in approximately 85% of patients, but stellate ganglion block (SGB) may fail to fully interrupt the sympathetic neural innervation of the head, neck, upper extremity, and upper thorax for several reasons. Although limited spread of local anesthetic may potentially fail to deliver agent onto disunited sympathetic ganglia, the presence of these sympathetic ganglia within the same fascial plane makes this unlikely.23 The distribution of radiographic contrast agent or dye in cadaveric studies demonstrates that injected volumes of 5 to 10 mL are routinely adequate to envelop the ganglion and may extend as far caudad as the T2 vertebral level.24,25 The nerve(s) of Kuntz are ascending ramus communicans branches originating at T2, T3, or T4 in 66% to 80% of individuals.26 These nerves are located approxi­ mately 7 mm from the sympathetic chain and provide an alternate pathway for sympathetic nerve fibers to bypass the sympathetic chain and enter directly into the first intercostal nerve or into the T1 nerve root. These Kuntz nerve fibers are not routinely bathed in local anesthetic agent during SGB and increased volumes of local anesthetic do not increase efficacy, but may produce undesirable spinal nerve root or brachial plexus block as well as unpredictable contralateral spread.

Indications Twentieth century medical literature records dozens of reported clinical series wherein SGB was performed for a variety of clini­ cal indications, all incorporating diagnostic or therapeutic appli­ cations where putative interruption of sympathetic afferent or

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efferent function of the head, neck, upper extremity, or thorax was postulated as useful. Present indications for SGB include the following27: Complex regional pain syndromes of head, neck, upper extremities ll Carotidynia ll Sympathetically mediated headache ll Cranial, cervical, nasal, orofacial, and upper extremity pain ­syndromes including peripheral neuralgias ll Hyperhidrosis ll Postthoracotomy pain ll Phantom or postamputation pain of the upper extremities ll Electrical shock injuries to the head, face, and upper extremity ll Vasospastic or vasoconstrictive syndromes of the head, neck, and upper extremity including Raynaud phenomenon ll After vascular injury or as an adjunct to surgical or interven­ tional procedures where vasospasm is anticipated or likely to be encountered ll Intractable angina ll Painful herpes zoster ll Intracranial vasospasm owing to cerebrovascular accident ll Treatment of postmenopausal “hot flashes” in women who have received chemotherapy28 ll

Contraindications Pregnancy, although contraindicating exposure to ionizing radia­ tion and fluoroscopy, may not prevent performance of SGB with ultrasound guidance; however, details of the ultrasound technique and potential obstetric issues are beyond the scope of this chap­ ter.29 Narrow angle glaucoma may be considered a contraindication owing to expectable miosis produced by the loss of sympathetic tone occurring with SGB. Recent myocardial infarction was formerly considered to represent a relative contraindication to SGB owing to risk of dys­ rhythmia. Newer evidence, however, supports sympathetic nerve sprouting and spontaneous increased sympathetic activity, which may follow myocardial infarction as a mechanism for sudden car­ diac death.30,31 A small experimental study of bilateral SGB in a rat coronary ischemia model demonstrated reduced ST segment eleva­ tions and substantially reduced incidence of ventricular tachycardia or fibrillation when compared to controls.32 Structural abnormalities such as a large goiter, skeletal defor­ mity, lymphadenopathy or neoplasm may recommend preoperative imaging and specific alternative techniques to achieve SGB, includ­ ing lateral or posterior approaches with which the operator may not be familiar.

Complications Widespread experience with SGB has produced descriptions of multiple, but fortunately infrequent, complications resulting from nonfluoroscopically guided SGB. These complications are largely predictable on an anatomic basis and include direct injury to adja­ cent structures, including hematoma producing neural compro­ mise; direct compression or deviation of the trachea; esophageal puncture; disc space entry; and pneumothorax. Inadvertent injec­ tion of local anesthetic into carotid or vertebral arteries is known to produce seizures. Venous or arterial injection of sufficiently large doses of local anesthetic can also result in cardiovascular collapse.

Local anesthetic blockade of adjacent neural structures can affect anesthesia of the recurrent laryngeal nerve, spinal nerve roots, brachial plexus, and epidural or intrathecal spaces producing anesthesia with consequences dependent on the particular neural structures anesthetized including bradycardia, hypotension, sen­ sory or motor functional loss, and total spinal anesthesia. Other adverse consequences of anesthetic blockade may include: Hoarseness or dysphagia owing to anesthetization of the recur­ rent laryngeal nerve ll Hypertension with anesthetic injection of the carotid sinus nerve ll Interruption of sympathetic tone (theoretically) producing car­ diac dysrhythmias, including bradycardia (see earlier) ll Infection including osteomyelitis of the vertebral body ll Discitis ll Horner syndrome ll

These should not be considered as complications but as expected side effects.

Technique (Fig. 42-1) A 5 mL volume of local anesthetic is sufficient for adequate SGB performed under fluoroscopy, CT,33 MRI, or ultrasound imaging.29 Evidence from cadaveric and in vivo studies suggests that larger vol­ umes (i.e., 20 mL) are neither necessary nor additionally efficacious because they often produce unwanted effects. Use of a 5 mL vol­ ume of bupivacaine 0.125%, bupivacaine 0.25%, or ropivacaine 0.2% minimizes risk of systemic local anesthetic toxicity. With any injection technique, a sterile 10 to 15 cm Luer-Lok small-bore extension tubing is attached to a three-way stopcock to which separate syringes of contrast agent and local anesthetic to be injected are attached. Syringes should be labeled or marked as to their contents. The assembly is primed with contrast agent and care should be taken to ensure that there is no remaining air in the tubing or syringes. The stopcock may be turned off to the extension tubing or open to the contrast agent, but in no case should this assembly be prepared with stopcock initially allowing the extension tubing to be filled with the local anesthetic. The syringe assembly should be constructed with aseptic technique and placed on a ster­ ile table or Mayo stand for ready access by the operator or a gloved assistant during the procedure. Anterior Paratracheal Technique Longstanding use of SGB has allowed description and experi­ ence with a variety of nonfluoroscopically guided techniques. The most common technique in present use is the anterior paratra­ cheal approach popularized by Moore and Bridenbaugh 50 years ago,34 now augmented by use of fluoroscopy for identification of anatomic landmarks instead of the traditional palpation of the transverse process of C6, as performed by earlier generations of anesthesiologists and neurosurgeons. For the anterior paratracheal technique, the patient is placed in a supine position on a radiolu­ cent operating table with a small (10 cm) folded towel roll placed between the dorsal scapulae with the head midline and cervical spine slightly extended. The arms are placed at the patient’s sides after appropriate physiologic monitors are applied. A small degree of head-up table tilt is often incorporated to reduce the distention of venous vasculature. The anterolateral cervical region is prepared with a suitable disinfectant agent, draped as the operator may pre­ fer, and aseptic technique is employed throughout the injection procedure.

Sympathetic Neural Blockade  511

Using midline anteroposterior (AP) fluoroscopic imaging, the cervical vertebrae are enumerated, the superior edge of the C6 vertebral body is squared off in planar fashion by adjustment of cephalocaudad beam angle and the transverse process of C6 is identified. The presence of cervical ribs may mislead the operator regarding the correct spinal level to be treated and careful enu­ meration is required. The carotid artery is palpated at the C6 level and the middle and index fingers of the operator’s gloved non­ dominant hand are inserted, angling dorsally to grasp the carotid sheath and its contents at the medial sheath border and to dis­ place these laterally by rotation of the hand on the wrist as the trachea and underlying esophagus are simultaneously displaced medially by the operator’s thumb. A 25-gauge, 2.5-inch, shortbevel tip needle is held in the dominant hand and visualized on intermittent fluoroscopy to overlie the proximal aspect of the ipsi­ lateral C6 transverse process, which should appear in the space between the operator’s thumb and index finger. A skin wheal of local anesthetic can be raised and the needle is then inserted and advanced directly posterior to contact the anterior aspect of the C6 transverse process near its junction with the vertebral body. Maintaining continuous contact of the needle tip against the bone to prevent needle dislodgement, the needle should be connected to the prepared Luer-Lok extension tubing, stopcock, and syringe assembly. After verification that the stopcock is turned open to the contrast agent and not to the local anesthetic, the needle is withdrawn 2 to 4 mm from the bony surface and held firmly with the hand while the contrast syringe, opened through the stopcock to the needle, is gently aspirated for blood or CSF. Withdrawal of the needle assures that the needle tip is not entirely invested in periosteum where flow cannot occur. Although withdrawing the needle tip as little as 2 mm may leave the needle tip within the longus colli muscle, the multi-pennate nature of this muscle will allow for flow of injectate within the musculofascial plane to reach the stellate ganglion. At the operator’s discretion, the operation of the stopcock and syringes may be delegated to an assistant. Negative aspira­ tion does not exclude entirely the possibility of intravascular injec­ tion and must be followed by live fluoroscopic observation of the resultant spread of 2 to 5 mL of radiographic contrast to confirm appropriate anatomic spread into a nonvascular paravertebral area with extraspinal pooling of injected contrast. Should blood or CSF be aspirated or should inappropriate vascular contrast distribu­ tion be observed or should contrast outline the radicular or ver­ tebral canals, no further injection should be made. The needle is disconnected from the syringe, stylet is inserted, and redirected prior to aspiration and contrast injection. After adequate distribu­ tion of radiocontrast is noted and documented in at least one, but preferably two radiographic planes, the stopcock is rotated open to the local anesthetic syringe and the local anesthetic is injected in aliquots of 2 to 5 mL with negative intermittent aspiration to a maximum volume of 5 to 10 mL. The needle is removed and gentle digital pressure is applied to obtain hemostasis. An adhesive ban­ dage may be applied. The postprocedure monitoring protocol is described subsequently. The principal hazards of the fluoroscopically guided anterior paratracheal technique are the lack of stabilization of the needle placement by passage through connective tissue or muscle and the routine direct exposure of the operator’s hands within the field of the x-ray fluoroscopic beam. Collimation of the beam is insuffi­ cient to manage radiation exposure to the operator. Although the operator can don leaded gloves in an attempt to mitigate direct

fluoroscopic beam exposure, the presence of lead attenuating the average beam energy at the image intensifier will cause many flu­ oroscopy units to automatically increase the beam energy deliv­ ered, ultimately increasing radiation exposure to the patient and substantially increasing the backscatter radiation exposure to the operator. Small-gauge needles are available that have a side orifice placed several mm proximal to the distal tip. The principle advantage of such a needle is that no withdrawal of the needle from the perios­ teal surface is necessary and the needle position remains stabilized throughout the procedure by continued bony contact rather than by the operator’s steadiness of hand. These needles typically have a blunted or pencil tip, requiring use of an introducer needle or use of a 20-gauge needle or scalpel blade to “pre-stick” the skin entry site to allow entry of the needle with a noncutting bevel. Lateral Approach Technique A more optimal technique for skilled interventionalists is the lat­ eral approach.35,36 This can be performed with the patient in the supine position with interscapular roll as described for the anterior paratracheal technique or with the patient placed in a semilateral “park bench” position on a radiolucent table. The initial approach is somewhat similar to that used for a C7 selective nerve root injec­ tion with anteroinferior adjustment of needle path to target the stel­ late ganglion. One advantage of the park bench position is that the needle axis is near-vertical allowing easy and familiar control of the needle trajectory by the physician. Excellent fluoroscopic visualization of the neural foramina is obtainable in this position. Optimal visual­ ization typically requires displacement of the dependent (“down”) shoulder inferiorly so that the contralateral humeral and clavicu­ lar shadow do not overlay or impede radiologic visualization of the ipsilateral C6-7 neural foramen. This is accomplished by manual downward pressure on the shoulder with only modest traction on the extremity. Park bench position will require additional time for positioning, padding, and securing the patient on the operating table and may require gentle manual traction on the nondependent extremity by an assistant. The sterile stopcock, extension set, and filled syringes are assembled and labeled as described earlier. Following antiseptic skin preparation and application of sterile drape, the C-arm fluoro­ scope is oriented initially to obtain a true AP image of the cervical spine. Subsequent cephalocaudad adjustment of the fluoroscope is used to level the C6-7 disc space, providing a crisp superior edge of the C7 vertebral body, which allows identification of the uncinate process at the cephalad aspect of the C7 body. The C-arm axis is then rotated ipsilaterally and obliquely about 30 to 50 degrees to bring the ipsilateral C6-7 neural foramen into direct en face view. In this view, the anteroinferior border of neural foramen formed by the anterior tubercle will be directly adjacent to or will minimally overlap the uncinate process of C7. The target is the midpoint of the linear junction of the ipsilateral uncinate process of C7 with the C7 vertebral body. The longus colli muscle fills the angular groove between the anterior tubercle and the vertebral body. After raising a skin wheal with local anesthetic, a 25-gauge, short bevel 2.5-inch needle is placed though the skin and advanced in small increments using intermittent fluoroscopy with rotation as needed to steer the needle to contact the target. A 5-degree bend away from the direction of the bevel in the distal 5 mm of the needle tip facilitates needle steering, but larger angulations or longer distal bent segments are best avoided because they produce larger and

42

512  Spine RT STELLATE GANGLION

RT STELLATE GANGLION

A

B RT STELLATE GANGLION

RT STELLATE GANGLION

C6-7 neural foramen

Anterior tubercle Uncinate process C7 body

C RT STELLATE GANGLION

D RT STELLATE GANGLION

Uncinate processes C5 C6 C7 T1

E

F

Figure 42-1  Stellate ganglion block: lateral approach. A, Oblique fluoroscopic view—needle on target point at junction between uncinate process and C7 vertebral body. B, Oblique view with drawn outline of relevant anatomic structures. C, Oblique view with labeled structures. D, Oblique view with injected contrast, 3 mL. E, Anteroposterior (AP) view with contrast. F, AP view with drawn and labeled uncinate processes. (Fluoroscopic images courtesy of Jeffrey D. Petersohn, MD.)

less predictable arcs of needle travel. The needle trajectory should be approximately parallel to the longitudinal axis of the interver­ tebral foramen, with direct entry into the neural foramen actively avoided to prevent inadvertent injection of the rare vertebral artery at C7 or the more frequently encountered radicular or medullary arteries. Avoiding entry into the foramen also prevents inadvertent nerve root or subdural injection as well as direct needle trauma to the spinal cord. Similarly, the needle should not stray cephalad

into the disc space or anteroinferiorly to avoid pleural trespass and subsequent pneumothorax. Straying too medial onto the anterior aspect of the vertebral body risks esophageal or tracheal entry. After the needle contacts the target point at the junction of the C7 body and the uncinate process, the needle is then withdrawn 1 mm and contrast agent is injected following negative aspiration as described earlier using the Luer-Lok tubing, stopcock, and syringe apparatus prepared previously.

Sympathetic Neural Blockade  513

Local distribution of injected contrast without vascular run­ off should be observed on live fluoroscopy and confirmed in the fluoroscopic AP view. Biplanar fluoroscopic images should be retained for documentation of technical adequacy of the proce­ dure. Evidence for vascular injection, seen as a “flash” of contrast on fluoroscopy or by visible pulsations of a rapidly running off of contrast agent, requires withdrawal of the needle and reassessment of the anatomy before further injection attempts are made. If there is no evidence of erroneous placement, the stopcock is then rotated and the local anesthetic is injected in aliquots as described earlier for the anterior paratracheal approach and the needle is removed. Postinjection care and monitoring protocols are described subse­ quently. The lateral technique provides superior stabilization of the needle by the sternocleidomastoid and the longus colli muscles. It allows improved avoidance of the carotid and vertebral arteries and does not require direct fluoroscopic exposure of the operator’s extremities. Postinjection Monitoring Protocol The patient is closely observed for ECG changes or seizure activity in the first few minutes after injection. Blood pressure and SaO2 are monitored in a standard postanesthesia protocol for at least 30 min­ utes postprocedure. Evaluation should be made for complications including pneumothorax, hematoma, hypotension or bradycardia, inadvertent intraarticular or intraspinal injection. Assessment of airway patency and signs or symptoms of sym­ pathetic neural blockade are made prior to discharge. Hoarseness or dysphagia is not uncommon due to recurrent laryngeal nerve anesthesia. Oral fluids should not be administered until the hoarse­ ness or dysphagia resolves. Assessment of Adequacy of SGB The monitoring of skin temperature differentials between upper extremities is often performed, but has not been established to be either a necessary or completely reliable finding of the onset of satisfactory sympathetic blockade. The development of a Horner syndrome [ptosis due to loss of sympathetic supply to the superior tarsal muscle, miosis (pupillary constriction), conjunctival injec­ tion, ipsilateral facial warmth, anhidrosis, ipsilateral vasodilation] is commonly taken to indicate a technically adequate SGB. Nasal stuffiness may be present, but does not reliably indicate adequacy of sympathetic blockade. As noted earlier, competent SGB may not produce complete sympatholysis because of an anatomic inability to interrupt sym­ pathetic fibers traveling outside the main sympathetic trunk. This may be more common in extremity pain syndromes and does not unequivocally constitute operator failure. If satisfactory sympa­ thetic blockade of the head and face occur, but the extremity is spared, consideration may be given to a single repetition of SGB, but repeated failure would suggest that other techniques, such as neural blockade of the sympathetic chain at T2, may be merited.

Sphenopalatine Ganglion Block Current indications for sphenopalatine ganglion block include the management of acute migraine, acute and chronic cluster head­ ache, and a variety of facial neuralgias, the classic example being vidian neuralgia. Permanent destruction of the sphenopalatine gan­ glion may be accomplished by creating a radiofrequency lesion in the ganglion37 or by use of the Gamma Knife.

Anatomy The sphenopalatine (pterygopalatine) ganglion resides in the ptery­ gopalatine fossa, located posterior to the middle nasal concha and anterior to the pterygoid canal. It is adjacent to and inferior to the maxillary nerve, a branch of the trigeminal nerve, and connects with it via the pterygopalatine nerves. Only parasympathetic fibers aris­ ing in the facial nerve synapse in the ganglion via fibers of the nerve of the pterygoid canal and the greater petrosal nerve. Postgangli­ onic fibers continue to the lacrimal, palatine, and nasal glands via orbital branches of the maxillary, lacrimal, and zygomatic nerves. Postganglionic sympathetic fibers originating in the internal carotid plexus pass through the ganglion (without synapsing) via the nerve of the pterygoid canal and the deep petrosal nerve. Sensory fibers connect the maxillary nerve to the ganglion by way of branches of the ganglion (primarily maxillary nerve fibers) that extend from the nasopharynx, nasal cavity, palate, and orbit. Five branches are usu­ ally described: The pharyngeal branch supplies the sphenoid sinus and the mucosa of the roof of the pharynx, the greater palatine nerve provides posterior inferior nasal branches that supply the palate via the greater palatine foramen (with components of the maxillary and facial nerves). The tonsil and soft palate are supplied via the lesser palatine nerve as it arises from the lesser palatine fora­ men. The nasopalatine nerve emerges through the sphenopalatine foramen, passes along the nasal septum, and emerges through the median incisive foramen to reach the hard palate. Posterior eth­ moid and sphenoid sinuses below the periosteum of the orbit are supplied via orbital branches. The nasal cavity is supplied via the posterior superior nasal branches. In addition to sensory fibers, the nasopalatine, palatine, and nasal nerves contain vasomotor fibers and secretory fibers to the palatine and nasal glands. Also, fibers related to taste can be found in the palatine nerves that pass via the greater petrosal nerve to reach the facial nerve.38

Technique (Fig. 42-2) The patient is placed supine. A cotton-tipped applicator soaked with viscous lidocaine 4% is advanced through the nares, along the middle turbinate posteriorly until it comes in contact with the pos­ terior wall of the nasopharynx. The zygomatic arch may be used as a landmark because it corresponds to the level of the middle turbinate. A second applicator is then generally placed somewhat posterior and superior to the initial one. A response is seen in 5 to 10 minutes, although it may be left in position for 30 minutes for an adequate evaluation of the block’s effectiveness. Common side effects are tearing or lacrimation, bleeding, lightheadedness, gen­ eralized discomfort, and complaints of numbness of the posterior oropharynx.39,40 Pterygopalatine fossa anesthetic block typically is done under fluoroscopy with the patient in the supine position. A true lat­ eral view is obtained with the head rotated to produce superim­ position of the right and left rami of the mandible, zygoma, and lateral pterygoid plates. The pterygopalatine fossa is most clearly visualized in this view as an “upside down vase.” A 22-gauge, B-bevel needle is inserted anterior to the mandible in the con­ dylar notch between the condylar and coronoid processes and under the zygoma and directed in a medial and slightly posterior direction with continuous visualization under fluoroscopy as it is advanced into the pterygopalatine fossa until it comes in con­ tact with the pterygoid plate. Paresthesias may be elicited if the

42

514  Spine

A

B

Figure 42-2  Sphenopalatine ganglion block. A, Anteroposterior (AP) view. B, Lateral View: Needle target on lateral view is occasionally referred to as an ‘Inverted flower vase’. (Images courtesy of Ted Kline, MD.)

needle impinges on the nasopalatine, greater or lesser palatine, or maxillary nerves. The C-arm is rotated in the anteroposterior view so that the tip of the needle is seen just under the lateral nasal mucosa. Approximately 1 mL of contrast agent may then be injected to check for venous runoff, because this is a highly vascular area. Needle position may be additionally confirmed by passing a small amount of electrical current through an insulated needle using a frequency of 50 Hz (sensory) and 2 Hz (motor) and low voltage (<1 volt). Stimulation may provoke some palatal or facial paresthesia but should not cause muscular twitching or paresthesia in other areas. Following successful stimulation 1 mL of 2% lidocaine or 0.25% bupicacaine is injected. Elimination of pain confirms the diagnosis. Dual sphenopalatine ganglion blocks can be used for diagnosis prior to use of stereotactic Gamma Knife lesioning technique.41,42 This avoids risks of repetitive instrumentation of this highly vascu­ lar area. Excellent landmarks for the sphenopalatine ganglion are obtained with coronal plane CT scan.

Radiofrequency Lesioning Technique A 100 mm, 22-gauge probe with a 2-mm active electrode tip is placed in the same way as described for pterygopalatine fossa anesthetic block. After needle contact with the pterygoid plate in the pterygopalatine fossa, sensory electrical stimulation is per­ formed up to 1 volt at 50 Hz. Correct stimulation is obtained when the patient reports the sensation to be within or just pos­ terior to the nose. If stimulation is achieved in the soft palate, the needle should be advanced slightly medially. To confirm that the probe is placed in an extravascular position, a 1-mL of con­ trast is injected. After confirmation of the extravascular position 1 mL of 2% lidocaine is injected. Following successful relief of symptoms, radiofrequency lesioning may be carried out for 60 seconds while maintaining the probe temperature above 65° C. The probe is then advanced 1 mm medially and the process is repeated. Generally the patient should be kept for observation after the procedure for approximately 2 hours, because 10% to 20% of patients experience epistaxis. Discomfort for 10 days to 2 weeks is expected. Loss of sensation on the soft palate also may occur. Addi­ tional complications are rare.37

Celiac Plexus and Splanchnic Nerve Block Indications for celiac plexus block include use as a diagnostic tool to determine whether flank, retroperitoneal, or upper abdominal pain is mediated via the celiac plexus, to palliate pain secondary to acute pancreatitis and intraabdominal malignancies, and to reduce the pain of abdominal “angina” associated with visceral arterial insufficiency.43-47 Strictly speaking, the celiac plexus is a mixed sympathetic and parasympathetic plexus with most of the sympathetic component provided by the greater and lesser splanchnic nerves. Neurolysis of the celiac plexus with alcohol or phenol is indicated to treat pain secondary to malignancies of the retroperitoneum and upper abdo­ men, but is usually avoided in chronic benign abdominal pain syn­ dromes, such as chronic pancreatitis, because the durability of relief is several months only. Although it is technically more challenging, advantages to splanchnic nerve block include an exclusively retro­ peritoneal approach, which reduces pneumothorax risk; ability to guide RF lesioning with stimulation mapping; and the absence of painful neuritis caused by unwanted neurolytic agent spreading to the somatic nerve roots. All usual contraindications to major neuraxial blockade apply to these procedures with the addition of bowel obstruction because increased motility and diarrhea can result from establishment of adequate neural blockade. Use of alcohol as a neurolytic agent should be avoided in patients on disulfiram therapy for alcohol abuse.

Anatomy Sympathetic innervation of the abdominal viscera originates in the anterolateral horn of the spinal cord, but fibers do not synapse until reaching the celiac plexus. Preganglionic fibers from T5-12 exit the spinal cord in conjunction with the ventral roots to form white communicating rami and the greater, lesser, and least splanchnic nerves which provide principal preganglionic (sympathetic) con­ tributions to the celiac plexus. The greater splanchnic nerve has its origin from the T5-10 spinal roots, travels along the thoracic paravertebral border, through the crus of the diaphragm and into the abdominal cavity, terminating on the ipsilateral celiac ganglion.

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The lesser splanchnic nerve arises from the T10-11 roots and passes with the greater splanchnic nerve to the celiac ganglion. The least splanchnic nerve arises from the T11-12 spinal roots and passes through the diaphragm to the celiac ganglion. Greater, lesser, and least splanchnic nerves are preganglionic structures that synapse at the celiac ganglia.46 Blockade of these nerves is properly termed splanchnic nerve block. Celiac Ganglia The three splanchnic nerves synapse at the celiac ganglia, which lie anterior and anterolateral to the aorta. The number of ganglia in the celiac plexus ranges from one to five and from 0.5 to 4.5 cm in diameter.48 Left-sided ganglia are typically more inferior than their right-sided counterparts by as much as a vertebral level, but both groups of ganglia are inferior to the level of the celiac artery. In most instances, the ganglia lie approximately at the level of the first lumbar vertebra. Postganglionic fibers form a diffuse perivascular plexus along blood vessels that supply abdominal viscera and are derived from the embryonic foregut.49 This includes distal esopha­ gus, stomach, duodenum, small intestine, ascending and proximal transverse colon, the adrenal glands, pancreas, spleen, liver, and biliary system. Celiac Plexus The celiac plexus arises from the preganglionic splanchnic nerves, vagal preganglionic parasympathetic fibers, sensory fibers from the phrenic nerve, and postganglionic sympathetic fibers.50 The celiac plexus is anterior to the diaphragmatic crura.51 It extends in front of and around the aorta, with the greatest concentration of fibers anterior to the aorta. Blockade of these neural structures, which include the afferent fibers carrying nociceptive information, is properly termed celiac plexus block. Note that the phrenic nerve also transmits nociceptive information from the upper abdominal viscera that may be perceived as poorly localized pain referred to the supraclavicular region.50 The normal configuration of these structures may be altered due to organomegaly or tumor. The aorta lies anterior and slightly to the left of the anterior margin of the vertebral body. The infe­ rior vena cava lies to the right of the midline, and the kidneys are posterolateral to the great vessels. The pancreas lies anterior to the celiac plexus. All of these structures lie within the retroperitoneal space.

Celiac Plexus Block The patient is placed in the prone position with a pillow beneath the abdomen to reverse the thoracolumbar lordosis, which increases the distance between the costal margins and the iliac crests as well as between the transverse processes of adjacent vertebral bodies. The patient’s spine is surveyed under fluoroscopic visualization. The lumbosacral junction and thoracolumbar junction, and lum­ bar vertebrae are enumerated. T12 ribs are identified. Anatomic anomalies are noted so that appropriate adjustments may be made. Beginning with a true AP fluoroscopic image, the C-arm is rotated to a posterolateral projection, stopping as the ipsilateral tip of L1 aligns with the lateral border of the of the L1 vertebral body. This angle will be between 30 and 45 degrees from the sagittal plane. If the ipsilateral T12 rib is superimposed on the L1 vertebral body, the C-arm should be rotated in a caudad to cephalad manner to just resolve this superimposition. Skin entry is made with a 6-inch, 22or 25-gauge needle with 10-degree distal curve to facilitate steering

just lateral to the junction of the L1 transverse process with the body after local anesthetic is infiltrated in the skin using the lateral L1 vertebral body as a target. After the needle tip contacts bone, the C-arm is rotated back to an AP projection to demonstrate a needle tip at the ipsilateral longitudinal interpedicular line. Cross table lat­ eral fluoroscopy should show the needle tip at the anterior vertebral body. At this point, the needle is rotated and aspirated in all four quadrants and 4 to 6 mL of nonionic contrast agent is injected. The contrast should remain immediately anterior to the anterior verte­ bral line on cross table lateral view, superimposed on the ipsilateral interpedicular line on sagittal view, and without vascular uptake. If the contrast column extends in an inferolateral projection on sagit­ tal view, the needle tip remains too lateral and should be cautiously advanced 1 cm medially, taking care not to penetrate a major vessel. A bend on the end of the needle as described will aid appropriate placement of the needle in this situation. If the contrast column is whisked away in a longitudinal fashion, the needle tip is in a major vessel and should be withdrawn slightly and contrast should be rein­ jected. If this does not correct the migration of the contrast column, needle placement should be reexamined and probably repeated. If the contrast column runs off in a serpentine fashion, the needle tip lies within Batson plexus and should be repositioned. If the needle tip cannot be repositioned to allow for appropriate contrast column as described, the procedure should be repeated. After the needle is appropriately placed as demonstrated by both contrast injection and radiographic evaluation, 10 mL of 1%  lidocaine or 0.25% bupivacaine is administered in divided ali­ quots. Local anesthetics should be administered in incremental doses.52 For treatment of the pain of acute or chronic pancreatitis, the historical practice of adding a depot steroid to the local anes­ thetic used for celiac plexus or sympathetic block is not presently supported by data.

Splanchnic Nerve Block Splanchnic nerve block may provide relief of pain in a subset of patients who fail to obtain relief from celiac plexus block.49,54 The splanchnic nerves transmit the majority of nociceptive informa­ tion from the viscera54 and are contained in a narrow compartment made up of the vertebral body and the pleura laterally, the posterior mediastinum ventrally, and the pleural attachment to the vertebra dorsally. This compartment is bounded caudally by the crura of the diaphragm. The volume of this compartment is approximately 10 mL on each side.54 The technique for splanchnic nerve block differs little from the approach to the celiac plexus, except that the needle is placed more cephalad to ultimately rest at the anterolateral margin of the T12 vertebral body. Needle placement medially against the vertebral body reduces the incidence of pneumothorax. An alternate approach to splanchnic nerve block uses 31⁄2- or 6-inch, 22-gauge spinal needles.55 The needles are placed 3 to 4 cm lateral to the midline just below the 12th ribs. Their trajectory is slightly mesiad so that their tips come to rest at the anterolateral margin of the T12 body. Complications of these techniques include hypotension, altered (increased) gastrointestinal motility, paresthesias or deficits of the lumbar somatic nerve, intravascular injection (venous or arte­ rial), subarachnoid or epidural injection, diarrhea, renal and other visceral injury, paraplegia, pneumothorax, chylothorax, pleural effusion, vascular thrombosis or embolism, vascular trauma, perfo­ ration of cysts or tumors, injection of the psoas muscle, intradiscal

42

516  Spine

injection, abscess, peritonitis, retroperitoneal hematoma, urinary abnormalities, ejaculatory failure, postprocedure pain, and failure to relieve pain.

Lumbar Sympathetic Block Anatomy Preganglionic sympathetic outflow to the lower extremity origi­ nates in the nerves of the lower thoracic and first two lumbar seg­ ments. Within the ventral rami of the nerve roots, small myelinated fibers form the white rami communicans; these preganglionic fibers synapse with small unmyelinated fibers in the ganglia of the lumbar sympathetic chain ganglia.56-58 The lumbar sympathetic ganglia lie along the anterolateral surface of the lumbar vertebrae just ante­ rior to the prevertebral fascia of the psoas muscle. The number of lumbar sympathetic chain ganglia varies considerably from one individual to another.56,57 Postganglionic fibers exit the ganglia as gray rami communicantes and supply one or more lumbar nerve roots. Deposition of local anesthetic along the sympathetic chain of the L2 or L3 levels will provide sympathetic denervation of the lower extremity.60 Bilateral blockade is not recommended due to the potential for significant hypotension.

Technique (Fig. 42-3) The patient’s lower thoracic and upper lumbar region is prepped in a sterile fashion. The patient is positioned prone. The fluoroscopic beam is rotated until the tip of the ipsilateral L2 transverse process is completely superimposed on the lateral border of the L2 vertebral body forming the target entry point. The needle is advanced until the needle tip gently contacts the inferior anterolateral L2 vertebral body.2,59,60 A cross table lateral view is taken, and the needle tip should be at the anterior vertebral line at the inferior L2 or superior L3 vertebrae. A sagittal view is obtained and the needle tip should be within the ipsilateral longitudinal interpedicular line. At this point 4 to 6 mL of nonionic contrast is injected, and the contrast column should extend up and down the ipsilateral thoracolumbar spine. On lateral view, the column remains immediately anterior to the anterior longitudinal line. A contrast column that extends in

A

B

a caudal and lateral direction is outlining the psoas muscle, which generally will provide a suboptimal sympathetic block and often will also block the anterior rami of the upper lumbar region. As a result, when a psoas shadow is seen, the needle should be advanced slightly and contrast should be reinjected. A vascular pattern should not be seen. If a suboptimal contrast column or a vascular pattern occurs and the needle cannot be manipulated to obtain correct placement, the procedure should be aborted.61 After both radiographic and contrast injection have confirmed correct needle placement, 10 to 15 mL of 0.25% bupivacaine is slowly injected.2,5 Successful sympathetic blockade is indicated by a rise in lower extremity temperature of at least 3° C.59 Complications Potential complications of LSB include intravascular injection, intradural injection with spinal anesthesia, postural headache, hypotension, lumbar plexus block, renal puncture, or genitofemo­ ral neuralgia.2,58,59 Postprocedural Care After successful SGB or LSB has been performed, it is important to carefully examine the involved extremity for resolution of pain or pain-producing stimuli. Significant reduction of pain (>50% to 75%) or painful stimuli in the absence of somatic blockade suggests the presence of SMP. Serial diagnostic blocks may be required to rule out a placebo response. Patients whose pain returns following a pain-free interval with SGB or LSB may be candidates for treatment with serial blocks. Additionally, arranging for the patient to participate in physical therapy for limb mobilization immediately following a successful block may greatly enhance the long-term treatment benefits of sympathetic blockade. Unfortunately, little controlled data exist to indicate the optimal frequency or ultimate number of serial blocks that are indicated in the management of SMP.

Superior Hypogastric Plexus Block Indications for this procedure include the diagnosis and treatment of pelvic pain originating from malignancy, endometriosis, pelvic inflammatory disease, adhesions, and other pathologic processes.

C

Figure 42-3  A through C, lumbar sympathetic nerve block at left L1, L2 and L3 levels. A single injection can be performed, most commonly at L1 or L2 using a 10 mL injectate volume. (Images courtesy of Way Yin, MD.)

Sympathetic Neural Blockade  517

The block was introduced in 1990, and several studies show good relief of intractable pelvic pain.62-64 However, as is the case for most of these procedures, the evidence for efficacy is low grade, suggest­ ing that superior hypogastric plexus block should be recommended as alternative and not as primary therapy.65 Contraindications are similar to those listed for the aforementioned procedures and include infection, sepsis, and coagulopathy.

Anatomy The superior hypogastric plexus is a retroperitoneal structure located bilaterally at the level of the lower third of the fifth lumbar vertebral body and upper third of the first sacral vertebral body at the sacral promontory and in proximity to the bifurcation of the common iliac vessels.66 This plexus (sometimes referred to as the presacral nerve) is formed by the confluence of the lumbar sympa­ thetic chains and branches of the aortic plexus that contains fibers that have traversed the celiac and inferior mesenteric plexuses. In addition, it usually contains parasympathetic fibers that originate in the ventral roots of S2-4 and travel as the slender nervi erigentes (pelvic splanchnic nerves) through the inferior hypogastric plexus to the superior hypogastric plexus. The superior hypogastric plexus divides into the right and left hypogastric nerves that descend lateral to the sigmoid colon and rectosigmoid junction to reach the two inferior hypogastric plex­ uses. The superior plexus gives off branches to the ureteric and testicular (or ovarian) plexuses, the sigmoid colon, and the plexus that surrounds the common and internal iliac arteries. The inferior hypogastric plexus is a bilateral structure situated on either side of the rectum, lower part of the bladder, and (in the male) prostate and seminal vesicles or (in the female) uterine cervix and vaginal forni­ ces. In contrast to the superior hypogastric plexus, which is situ­ ated in a predominantly longitudinal plane, the configuration of the inferior hypogastric plexus is oriented more transversely, extend­ ing posteroanteriorly and parallel to the pelvic floor. Because of its location and configuration, the inferior hypogastric plexus does not lend itself to surgical or chemical extirpation.

Technique The patient is placed in the prone position with a pillow under the pelvis to reduce lumbar lordosis. The lumbosacral region is cleansed aseptically. The lumbar region is surveyed under fluoroscopy. The fluoroscopy tube is rotated approximately 45 degrees for a postero­ lateral view of the L5 vertebral body. At this point, an image of the iliac crest will most likely be superimposed on the L5 vertebral body. The fluoroscopy tube is then rotated in a cephalad-caudad direction (the appropriate view is posterolateral and cephalad to caudad) so that the image of the iliac crest is no longer superimposed on the L5 vertebral body. At this point a 31⁄2- or 6-inch, 22- or 25-gauge spinal needle is inserted using an en pointe method down to the anterolateral L5 vertebral body. The fluoroscopic image is rotated in a sagittal plane and cross table manner. In the sagittal plane, the needle tip should lie in the ipsilateral longitudinal interpedicular line, and in the cross table lateral view the needle tip should rest at the anterior longitudinal line. If the needle repeatedly encounters the L4 or L5 transverse processes, a slightly more axial trajectory requiring repeated biplanar fluoroscopic views to properly place the needle may be necessary. If this method fails, a 30-degree bend should be placed in the needle 1 to 2 cm from the end of the needle with the convexity on the bevel side of the needle. By alternately

rotating the needle while the needle is advanced, the needle tip may be steered around anatomic impediments. After fluoroscopic visu­ alization confirms needle placement, 2 to 4 mL of nonionic contrast agent should be injected. The contrast column should remain along the midline or paramedian region in the sagittal view and the pre­ vertebral space in the cross table lateral view. For diagnostic blocks, 8 mL of 0.25% bupivacaine or 1% lidocaine is injected. Complications Vascular puncture with risks of subsequent hemorrhage and hema­ toma formation is possible because of the proximity of the bifurca­ tion of the common iliac vessels. Intramuscular or intraperitoneal injection may result from an improper estimate of needle depth. These and less likely complications (e.g., subarachnoid and epidural injection, somatic nerve injury, renal or ureteral puncture) can be avoided by diligent technique and frequent fluoroscopic views dur­ ing needle placement.

Ganglion Impar Block Anatomy The ganglion impar, also known as the ganglion of Walther, is the uniquely unpaired caudad terminus of the bilateral sympathetic chains and provides sympathetic innervation to the perineum.67,68 The ganglion is typically about 0.5 cm in length and is located in the midline, anterior to the first and second coccygeal vertebra and dorsal to the rectum.

Indications Ganglion impar block (GIB) is used to treat chronic, recalcitrant perineal or pericoccygeal pain when it is considered that there is a sympathetic or neuropathic component to the pain. Thus, local symptoms might include burning pain and signs include cutaneous allodynia and hyperalgesia. Specific conditions for which it is used include SMP or CRPS I/II of perineum, coccygodynia, and perineal hyperhidrosis.

Contraindications Pregnancy, although contraindicating exposure to ionizing radia­ tion and fluoroscopy, may not prevent performance of GIB with ultrasound guidance; however, details of the ultrasound technique and potential obstetric issues are beyond the scope of this chapter.

Technique There are two general techniques described for GIB: trans-discal or trans-anococcygeal ligament approach. In the trans-discal approach, a 22- or 25-gauge 1 to 1.5” single or double needle is inserted in the midline just through the sacrococcygeal, first inter­ coccygeal or second intercoccygeal joint. In the trans-anococcy­ geal ligament approach a single curved needle is inserted through the midline ano-coccygeal ligament and advanced against the anterior midline concavity of the inferior sacrum and coccyx to contact the ventral coccyx. The disadvantage of the former tech­ nique may include difficulty placing the needle into or through a calcified joint space. The disadvantage of the trans-anococcygeal ligament techniques is the risk of infection posed by adjacency to

42

518  Spine

the rectum and the risk of rectal perforation and bleeding owing to the longer needle course. Commonly used anesthetic agents include bupivacaine in 0.25% concentrations. A volume of 2 to 4  mL of contrast is typically sufficient to document satisfactory injection technique. If RF lesioning is contemplated, a pair of 20-gauge curved RF needles are used with 10 mm active tips placed parallel to and straddling the midline, just anterior to the coccyx about 5 to 6 mm apart. A bipolar strip lesion can be created at temperatures of 70 to 80° C for 90 seconds. Assessment of pain and function should be documented postoperatively including the proportion and ultimate duration of improvement that follows each GIB.

Complications Potential adverse effects include infection of subcutaneous or deep tissues, including discs/joints at sacrococcygeal or intercoccygeal junctions, rectal perforation, and bleeding. REFERENCES   1. Racz GB, Heavener JE, Noe CE. Definitions, classifications and taxon­ omy: An overview. Phys Med Rehabil State Art Rev. 1996;10:195-206.   2. Lofstrom J, Cousins MJ. Sympathetic neural blockade of the upper and lower extremity. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesia and Management of Pain. Philadelphia: JB Lippincott; 1988:461.   3. Mandel S, Rothrock R. Sympathetic dystrophies: Recognizing and man­ aging a puzzling group of syndromes. Postgrad Med. 1990;87:213-218.   4. Stanton-Hicks M. Upper and lower extremity pain. In: Raj P, ed. ­Practical Management of Pain. St Louis: Mosby; 1991:312.   5. Charlton JE. Management of sympathetic pain. Br Med Bull. 1991;47:601-618.   6. Maihofner C, Baron R, DeCol R, et al. The motor system shows adaptive changes in complex regional pain syndrome. Brain. 2007;130:2671-2687.   7. Maihofner C, Forster C, Birklein F, et al. Brain processing during mechanical hyperalgesia in complex regional pain syndrome: A func­ tional MRI study. Pain. 2005;114:93-103.   8. Freund W, Wunderlich AP, Stuber G, et al. Different activation of oper­ cular and posterior cingulate cortex (PCC) in patients with complex regional pain syndrome (CRPS I) compared with healthy controls dur­ ing perception of electrically induced pain: A functional MRI study. Clin J Pain. 2010;26:339-347.   9. Kozin F, Soin JS, Ryan LM, et al. Bone scintigraphy in the reflex sympa­ thetic dystrophy syndrome. Radiology. 1981;138:437-443. 10. Smith FJ, Powe JE. Effect of sympathetic blockade on bone imaging. Clin Nucl Med. 1992;17:665-669. 11. Werner R, Davidoff G, Jackson MD, et al. Factors affecting the sensitiv­ ity and specificity of the three-phase technetium bone scan in the diag­ nosis of reflex sympathetic dystrophy syndrome in the upper extremity. J Hand Surg Am. 1989;14:520-523. 12. Raja SN, Davis KD, Campbell JN. The adrenergic pharmacology of sym­ pathetically-maintained pain. J Reconstr Microsurg. 1992;8:63-69. 13. Kumar K, Nath RK, Toth C. Spinal cord stimulation is effective in the management of reflex sympathetic dystrophy. Neurosurgery. 1997;40:503-508. 14. Suseki K, Takahashi Y, Takahashi K, et al. Innervation of the lumbar facet joints. Origins and functions. Spine. 1997;22:477-485. 15. Tubbs RS, Loukas M, Remy AC, et al. The vertebral nerve revisited. Clin Anat. 2007;20:644-647. 16. Oh WS, Shim JC. A randomized controlled trial of radiofrequency denervation of the ramus communicans nerve for chronic discogenic low back pain. Clin J Pain. 2004;20:55-60. 17. Simpson EL, Duenas A, Holmes MW, et al. Spinal cord stimulation for chronic pain of neuropathic or ischaemic origin: Systematic review and economic evaluation. Health Technol Assess. 2009;13:iii, ix-x,154.

18. Murata Y, Kato Y, Miyamoto K, et al. Clinical study of low back pain and radicular pain pathways by using L2 spinal nerve root infiltration: A randomized, controlled, clinical trial. Spine. 2009;34:2008-2013. 19. Richardson J, Collinghan N, Scally AJ, Gupta S. Bilateral L1 and L2 dorsal root ganglion blocks for discogenic low-back pain. Br J Anaesth. 2009;103:416-419. 20. Lang J. Clinical Anatomy of the Cervical Spine. New York: Thieme; 1993. 21. Marples IL, Atkinson RE. Stellate ganglion block. Pain Reviews. 2001;8:3-11. 22. Pather N, Partab P, Singh B, Satyapal KS. Cervico-thoracic ganglion: Its clinical implications. Clin Anat. 2006;19:323-326. 23. Honma M, Murakami G, Sato TJ, Namiki A. Spread of injectate during C6 stellate ganglion block and fascial arrangement in the prevertebral region: An experimental study using donated cadavers. Reg Anesth Pain Med. 2000;25:573-583. 24. Feigl GC, Rosmarin W, Stelzl A, et al. Comparison of different injectate volumes for stellate ganglion block: An anatomic and radiologic study. Reg Anesth Pain Med. 2007;32:203-208. 25. Guntamukkala M, Hardy PA. Spread of injectate after stellate ganglion block in man: An anatomical study. Br J Anaesth. 1991;66:643-644. 26. Chung IH, Oh CS, Koh KS, et al. Anatomic variations of the T2 nerve root (including the nerve of Kuntz) and their implications for sympa­ thectomy. J Thorac Cardiovasc Surg. 2002;123:498-501. 27. Hamann W, di Vadi PP. The clinical role of sympathetic blocks. Pain Reviews. 1999;6:314-321. 28. Lipov EG, Joshi JR, Sanders S, et al. Effects of stellate-ganglion block on hot flushes and night awakenings in survivors of breast cancer: A pilot study. Lancet Oncol. 2008;9:523-532. 29. Narouze S, Vydyanathan A, Patel N. Ultrasound-guided stellate gan­ glion block successfully prevented esophageal puncture. Pain Physician. 2007;10:747-752. 30. Chen LS, Zhou S, Fishbein MC, Chen PS. New perspectives on the role of autonomic nervous system in the genesis of arrhythmias. J ­Cardiovasc.Electrophysiol. 2007;18:123-127. 31. Chen PS, Chen LS, Cao JM, et al. Sympathetic nerve sprouting, electrical remodeling and the mechanisms of sudden cardiac death. C ­ ardiovasc Res. 2001;50:409-416. 32. Yang Z, Abdi S. Bilateral stellate ganglion block attenuates myocardial ischemia and ventricular arrhythmias. J Pain. 2005;6:S23. 33. Erickson SJ, Hogan QH. CT-guided injection of the stellate gan­ glion: Description of technique and efficacy of sympathetic blockade. ­Radiology. 1993;188:707-709. 34. Moore DC, Bridenbaugh Jr LD. The anterior approach to the stellate ganglion use without a serious complication in two thousand blocks. J Am Med Assoc. 1956;160:158-162. 35. Abdi S, Zhou Y, Doshi R, Patel N. Stellate ganglion block: Emphasis on the new oblique fluoroscopic approaches. Tech Reg Anesth Pain Manag. 2005;9:73-80. 36. Abdi S, Zhou Y, Patel N, et al. A new and easy technique to block the stellate ganglion. Pain Physician. 2004;7:327-331. 37. Kline M. Stereotactic Radiofrequency Lesions as Part of the Management of Pain. Orlando, Fla: Paul M Deutsch Press; 1992:54. 38. Gardner G, Gray AJ, O’Rahilly SF. Anatomy: A Regional Study of Human Structure. 5th ed. Philadelphia: WB Saunders; 1906:676-677. 39. Bridenbaugh MJ, Cousins PO. Neural Blockade in Clinical Anesthesia and Management of Pain. Philadelphia: JB Lippincott; 1988:543. 40. Ramamuithy S, Rogers J, eds. Decision Making in Pain Management. St Louis: Mosby; 1993:258-259. 41. Kano H, Kondziolka D, Mathieu D, et al. Stereotactic radiosurgery for intractable cluster headache: An initial report from the North ­American Gamma Knife Consortium. J Neurosurg. Epub ahead of print 30 Apr 2010. 42. Karas C, Baig MN, Larson T, et al. Merged imaging and expanded tar­ get selection in gamma knife radiosurgical ablation of the sphenopala­ tine ganglion. Stereotact Funct Neurosurg. 2008;86:127-131. 43. Dale WA. Splanchnic block in the treatment of acute pancreatitis. ­Surgery. 1952;32:605-614.

Sympathetic Neural Blockade  519 44. Loper KA, Coldwell DM, Lecky J, et al. Celiac plexus block for hepatic arterial embolization: A comparison with intravenous morphine. Anesth Analg. 1989;69:398-399. 45. Portenoy RK, Waldman SD. Recent advances in the management of cancer pain. Part I. Pain Management. 1991;4:23-29. 46. Raj PP. Chronic Pain. In: Raj PP, ed. Handbook of Regional Anesthesia. New York: Churchill Livingstone; 1985:113-115. 47. Waldman SD. Acute and postoperative pain. Management from a pri­ mary care perspective. Postgrad Med. 1992;18:15-17. 48. Ward EM, Rorie DK, Nauss LA, et al. The celiac ganglia in man: Normal anatomic variations. Anesth Analg. 1979;58:461-465. 49. Patt RB. Nuerolytic blocks of the sympathetic axis. In: Patt RB, ed. ­Cancer Pain. Philadelphia: JB Lippincott; 1993:393-411. 50. Bonica JJ. Autonomic innervation of the viscera in relation to nerve block. Anesthesiology. 1968;29:793-813. 51. Woodburne RT, Burkel WE. Essentials of Human Anatomy. New York: Oxford University Press; 1988p 552. 52. Waldman SD, Portenoy RK. Recent advances in the management of cancer pain. Part II. Pain Management. 1991;4:19. 53. Reference deleted in proofs. 54. Abram SE, Boas RA. Sympathetic and visceral nerve blocks. In: ­Benumof JL, ed. Clinical Procedures in Anesthesia and Intensive Care. Philadelphia: JB Lippincott; 1992:787. 55. Parkinson SK, Mueller JB, Little WL. A new and simple technique for splanchnic nerve block using a paramedian approach and 3 1/2-inch needles. Reg Anesth. 1989;14(Suppl):41. 56. Gray H. The peripheral nervous system. In: Clement C, ed. Anatomy of the Human Body. Philadelphia: Lea & Febiger; 1985:149. 57. Hollinshead H. The nervous system. Textbook of Anatomy. Hagerstown, Md: Harper & Row; 198437.

58. Schmidt SD, Gibbons JJ. Postdural puncture headache after fluoroscop­ ically guided lumbar paravertebral sympathetic block. Anesthesiology. 1993;78:198-200. 59. Sprague RS, Ramamurthy S. Identification of the anterior psoas sheath as a landmark for lumbar sympathetic block. Reg Anesth. 1990;15:253-255. 60. Umeda S, Arai T, Hatano Y, et al. Cadaver anatomic analysis of the best site for chemical lumbar sympathectomy. Anesth Analg. 1987;66:643-646. 61. Rocco AG. Radiofrequency lumbar sympatholysis. The evolution of a technique for managing sympathetically maintained pain. Reg Anesth. 1995;20:3-12. 62. Bosscher H. Blockade of the superior hypogastric plexus block for vis­ ceral pelvic pain. Pain Pract. 2001;1:162-170. 63. Plancarte R, Amescua C, Patt RB, Aldrete JA. Superior hypogastric plexus block for pelvic cancer pain. Anesthesiology. 1990;73:236-239. 64. Plancarte R, de Leon-Casasola OA, El-Helaly M, et al. Neurolytic supe­ rior hypogastric plexus block for chronic pelvic pain associated with cancer. Reg Anesth. 1997;22:562-568. 65. Schmidt AP, Schmidt SR, Ribeiro SM. Is superior hypogastric plexus block effective for treatment of chronic pelvic pain? Rev Bras ­Anestesiol. 2005;55:669-679. 66. Pitkin G, Southworth JL, Hingson RA, et al. Anatomy of the sympathetic trunk. Conduction Anesthesia. 2nd ed. Philadelphia: JB Lippincott; 1953. 67. Plancarte R, Amescua C, Patt R, et al. Presacral blockade of the ganglion of Walther (ganglion impar). Anesthesiology. 1990;73:751. 68. Plancarte R, Guajardo J, Lee A. On the true origins of the Walther’s ganglion blockade and more. Pain Pract. 2008;8:333-334.

42

Imaging for Chronic Spinal Pain

43

Timothy P. Maus, MD

Imaging is commonly considered an essential component in evaluation of the patient with back and/or neck pain. However, evidence of its effectiveness is often wanting. This chapter examines the literature support for imaging in the evaluation of pain of spinal origin, including the risk/benefit context as befits any medical procedure. Specificity and sensitivity shortcomings are also addressed. With this background, the strengths and weakness of various imaging modalities, and potential imaging strategies are then reasonably discussed. Back pain remains the most common and most expensive cause of work disability in the United States.1 Recent data suggest that approximately 26% of U.S. citizens have experienced low back pain, and 14% have experienced neck pain, within the past 3 months.2 The course of acute or persistent low back pain is not as optimistic as has been generally conveyed.3 Von Korff and colleagues studied patients with a recent (within 6 months) history of low back pain and found that at 6 months, 76% of patients either had no pain (21%) or mild pain and low disability, but that 14% had high disability with moderate-to-severe limitation of function.4 A British study of acute low back pain noted full recovery in only 21% and 25% at 3 and 12  months, respectively.5 A Dutch study found that 70% of acute low back pain patients still had pain at 4 weeks, with a median time to recovery of 7 weeks; however, back pain tended to persist with residual prevalence of 35% at 12 weeks and 10% at 1 year, and 76% sustained a median number of two relapses of pain within that 1 year.6 An Australian study was more encouraging; at 3 months 49% to 67% (two study groups) had recovered, at 12 months 56% to 71% had recovered, with a relapse rate within that 1 year of 7% to 27%.7 Back pain accounted for more than 890 million physician office visits in the United States in 2002; however, the back pain proportion of total physician visits has remained stable since the early 1990s.2 Despite this, utilization of imaging has increased dramatically; U.S. Medicare use of lumbar magnetic resonance imaging (MRI) rose 307% in the 12-year interval 1994 to 2005.8 Imaging utilization is often unreasoned. There are large variations in rates of imaging across the United States; from one-third to two-thirds of spine computed tomography (CT) and MRI studies are inappropriate when measured against established guidelines.8 The relatively unregulated U.S. medical marketplace has served as a laboratory for the mass consumption of imaging technology, with no detectable benefit in patient outcomes. Despite incurring the greatest per capita expenditures for the diagnosis and treatment of back pain, including dramatically increased use of imaging, the United States continues to have the highest rate of back painrelated work disability of all industrialized societies.

Within this disconcerting context, it is critical to remember that for most patients, back pain is self-limiting or associated with mild disability, and therefore does not require imaging or complex intervention. The proper role of imaging is to aid in the identification of that small proportion of back pain sufferers with systemic disease as the underlying cause of their pain, or neurologic compromise requiring intervention. It is well established that there is no role for imaging early in the course of a low back or limb pain syndrome. In a recent metaanalysis in Lancet, Chou and coworkers identified six randomized controlled trials evaluating the early use of imaging versus clinically directed care.9 In the pooled data, there were no significant outcome differences in pain or function in imaged versus nonimage patients in the short- (3 months) or long-term (6 to 12 months). These data apply primarily to acute or subacute back pain in primary care settings, and encompass radiographs and advanced imaging. Multiple studies have included economic analyses, which make it clear that radiographs obtained early in the course of a back pain syndrome are not cost effective; a study by Jarvik and associates suggested that radiographs performed on an initial visit for acute back pain in the absence of signs of systemic disease will ultimately cost $2000 (1982 U.S. dollars) to alleviate a single day of pain.1 A study by Carragee10 reinforced the futility of early advanced imaging. This 5-year prospective observational study obtained baseline MRI examinations on a large cadre of asymptomatic patients at risk for back pain due to strenuous vocations. These patients were then contacted periodically; when a subset ultimately presented to their physician with back or leg pain, a second lumbar MRI was performed. The study noted that fewer than 5% of the MRI scans obtained at the time of acute presentation showed clinically relevant new findings; the vast majority of the “abnormalities” were present on the imaging performed when the patient was asymptomatic. Only direct evidence of neural compression in patients with corresponding radicular pain syndromes was useful. Also of note, psychosocial factors were the primary predictors of the degree of disability, not the morphology identified on imaging.

Early Imaging Recommendations Based on such data, there is broad international consensus on the lack of efficacy of imaging in acute pain syndromes of spinal origin. The American College of Radiology11,12 considers that imaging is 521

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inappropriate in acute low back pain unless there are complicating (“red flag”) features including the following: 1. R  ecent significant trauma, or milder trauma, age >50 2. U  nexplained weight loss 3. U  nexplained fever 4. I mmunosuppression 5. H  istory of cancer 6. I V drug use 7. P  rolonged use of corticosteroids, osteoporosis 8. A  ge >70 9. F  ocal neurologic deficit with progressive or disabling symptoms 10. D  uration longer than 6 weeks Similarly, the Agency for Healthcare Research and Policy (U.S.) guidelines advises no imaging in patients younger than 50 years of age in the absence of systemic disease, or until pain persists for at least 4  weeks.13 The Australian National Health and Medical Research Council recommends against imaging in nonspecific low back pain of less than 12 weeks’ duration in the absence of red flag features suggesting underlying systemic disease.14 The American College of Physi­ cians and the American Pain Society released a joint guideline in 2007 stating that imaging should not be obtained in patients with nonspecific low back pain unless there is a severe or progressive neurologic deficit, or when serious underlying systemic disease is suspected.15 Furthermore, patients with signs or symptoms of radiculopathy or spinal stenosis should be imaged with MRI (preferred) or CT only if they are candidates for surgery or epidural steroid injection.15 The primary role of imaging in the back pain patient is to aid in the detection of systemic disease that is causal of back or back-related leg pain. In essence, imaging is undertaken to detect neoplasm, infection, or manifestations of unsuspected traumatic injury. In a patient presenting with back pain to a primary care physician, these conditions are highly uncommon. In this population, only 0.7% of patients will have metastatic neoplasm, 0.01% spine infection, 0.3% ankylosing spondylitis, and 4% will have osteoporotic compression fractures.1 The differential diagnosis of back pain, and the relative frequency of causal conditions, are displayed in Table 43-1.1 The imperfect sensitivity and specificity of all imaging modalities makes diagnostic accuracy problematic, given the low pretest probability of systemic disease. According to Jarvik and Deyo, there are three essential questions that must be answered for the patient with back pain: (1) is there evidence of underlying systemic disease? (2) Is there neurologic impairment requiring surgical intervention? (3) Are social/psychological factors exacerbating the pain? Imaging may help to identify systemic disease and anatomic neural impingement, but its role should not be overstated.1 As Jarvik and colleagues note, depression is a more significant predictor of new low back pain than MRI imaging findings.16

Risk/Benefit Analysis As with any medical procedure, a decision to proceed with imaging of the spine should involve a risk/benefit analysis. Certainly patients will benefit from imaging when it aids in the identification of previously undiagnosed systemic disease. In the setting

of progressive neurologic deficit, imaging can identify the neural compressive lesion and assist in planning surgical or minimally invasive interventions. Pain physicians performing interventional procedures must scrutinize available imaging to best plan access routes for medication or energy delivery. There should be benefit to the patient through reassurance in confirming the absence of sinister pathology. This is dependent on the pain physician actively educating the patient regarding the significance, or inconsequence, of imaging findings. Benefit should also accrue from stopping any further work-up. In patients whose pain becomes chronic, imaging may help in identification of the cause of chronic pain and allow institution of therapy specific to that process. There are, however, risks involved in imaging. These include the labeling effect, radiation exposure, monetary cost, and the provocation of intervention. The labeling effect refers to the inevitable identification of degenerative phenomenon on any spine imaging test. Degenerative findings on spine imaging are almost always inconsequential. If this is not made very clear to patients, they may identify themselves as suffering from a degenerative process from which there is no ultimate recovery. This can lead to fear avoidance behaviors, deconditioning, and depression. The pain practitioner is obligated to educate the patient that degenerative findings seen on imaging have little if any prognostic value, and actively contradict common misconceptions regarding back pain. A recent Cochrane review concluded that intensive patient education is effective in patients with acute and subacute low back pain; its value in chronic pain patients is less clear.17 The Australian media studies of Buchbinder also document the effectiveness of carefully planned educational efforts in changing patient and physician attitudes and reducing disability related to back pain.18 Radiation exposure from radiographs or CT must also be carefully considered. The effective radiation dose (biologic effect) is measured by the Sievert (Sv). The average natural background exposure is approximately 3.0 mSv per year.19 A three- view lumbar spine radiographic series exposes the patient to approximately 1.5 mSv; lumbar spine CT carries an exposure of approximate 6 mSv. An abdominal and pelvic CT delivers an average of 14 mSv; a technetium bone scan results in an average of 6.3 mSv exposure. Frontal and lateral chest radiographs, by contrast, expose the patient to 0.1 mSv.19 Radiation exposure is cumulative; repeated radiographic or CT examinations without clear expectation of patient benefit through improved decision-making cannot be condoned. Imaging is costly. In the United Kingdom, imaging is known to comprise approximately 5% of the direct medical costs related to back pain.20 This is likely significantly higher in the less regulated U.S. marketplace. The 2009 Medicare reimbursements for lumbar spine imaging in the United States are: lumbar radiographs, $36; lumbar spine CT (noncontrast), $241; CT myelography, $525; MRI (noncontrast), $402, and bone scan with SPECT, $239.21 Nominal fees may be three to five times Medicare reimbursements. These costs directly affect our patients and our society and should be incurred only through reasoned decision-making. Finally, imaging is likely to provoke intervention. Jarvik noted that early MRI imaging of the spine leads to increased surgical interventions despite equivalent pain and disability profiles when compared with nonimaged patients.22 Similarly, a study by Lurie and associates found that the intensity of CT and MRI use can account for virtually all of the extensive (12-fold) regional variation in surgical rates for spinal stenosis in the United States.23 When we image, we intervene. This occurs with standard of care interventions (many of which have little evidence basis) and totally

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Table 43-1  Differential Diagnosis of Low Back Pain* Mechanical Low Back or Leg Pain (97%)†

Nonmechanical Spinal Conditions (−1%)

Visceral Disease (2%)

Lumbar strain or sprain (70%)‡

Neoplasia (0.7%)

Pelvic organ involvement

Degenerative processes of disc and facets (usually related to age) (10%)

Multiple myeloma

Prostatitis

Herniated disc (4%)

Metastatic carcinoma

Endometriosis

Spinal stenosis (3%)

Lymphoma and leukemia

Chronic pelvic inflammatory disease

Osteoporotic compression fracture (4%)

Spinal cord tumors

Renal involvement

Spondylolisthesis (2%)

Retroperitoneal tumors

Nephrolithiasis

Traumatic fractures (<1%)

Primary vertebral tumors

Pyelonephritis

Congenital disease (<1%)

Infection (0.01%)

Perinephric abscess

Severe kyphosis

Osteomyelitis

Aortic aneurysm

Severe scoliosis

Septic discitis

Gastrointestinal involvement

Transitional vertebrae

Paraspinous abscess

Pancreatitis

Spondylolysis§

Epidural abscess

Cholecystitis

Internal disc disruption or discogenic back pain¶

Shingles

Penetrating ulcer

Presumed

instability**

Inflammatory arthritis (often HLA-B27 associated) (0.3%) Ankylosing spondylitis Psoriatic spondylitis Reiter syndrome Inflammatory bowel disease Scheuermann disease (osteochondrosis) Paget disease

*Diagnoses

in italics are often associated with neurogenic leg pain. Figures in parentheses indicate estimated percentage of patients with these conditions among all adult patients with signs and symptoms of low back pain. Percentages may vary substantially according to demographic characteristics or referral patterns in a practice. For example, spinal ­stenosis and osteoporosis will be more common in geriatric practices and spinal infection will be more common in injection drug users. †The term mechanical is used here to designate an anatomic or functional abnormality without an underlying malignant, neoplastic, or inflammatory disease. ‡Strain and sprain are nonspecific terms with no pathoanatomic confirmation. Idiopathic low back pain may be a preferable term. §Because spondylolysis is equally common in asymptomatic persons and those with low back pain, its etiologic role remains ambiguous. ¶Internal disc disruption is diagnosed by provocative discography (injection of contrast material into a degenerative disc, with assessment of pain at the time of injection). However, discography often generates pain in asymptomatic adults, and many patients with positive discogram results improve spontaneously. Thus, the significance and appropriate ­management of this disorder remain unclear. Discogenic back pain is often used synonymously with internal disc disruption. **Presumed instability is loosely defined as >10 degrees of angulation or 4 mm of vertebral displacement on lateral flexion and extension radiographs. However, diagnostic criteria, natural history, and surgical indications remain controversial. Data obtained from Deyo,4 Hart et al.,6 Deyo et al.,7 and Deyo et al.8 Reproduced with permission Deyo RA, Weinstein JN: Low back pain. N Engl J Med 2001;344:363-370. ­Copyright© 2001. Massachusetts Medical Society. All rights reserved.

unproven interventions with significant risks that have found their way into our highly imperfect medical marketplace. The single most important imaging precept in the back pain patient is this: treat the patient, do not treat the images.

Specificity and Sensitivity Considerations Having considered the relative risks and benefits, the clinician may choose to initiate imaging in the back pain patient. To best utilize the results of imaging endeavors, sensitivity and specificity shortcomings of all spine imaging modalities must be appreciated. Specificity shortcomings of spine imaging apply to all modalities from simple radiographs to the most elaborate MRI study, and have been well documented for decades. Hitselberger and associates noted in 1968 that myelographic studies were abnormal in 24% of asymptomatic volunteers.24 Wiesel and associates subsequently showed that CT demonstrated “significant” abnormalities in 50% of asymptomatic volunteers over the age of 40.25 Boden and associates

showed that MRI of asymptomatic volunteers over the age of 60 demonstrated “significant” findings in 57% of asymptomatic volunteers.26 Numerous studies of asymptomatic volunteers can be summarized as follows: (1) imaging demonstrates abnormalities in the lumbar spine of 1/3 to 2/3 of asymptomatic persons; (2) annular fissures, disc bulges or protrusions, facet degeneration, and lowgrade antero- or retrolisthesis are common, usually asymptomatic, and their prevalence increases with increasing age; (3) disc extrusions, severe central canal stenosis, and direct evidence of a neural compression are more likely to be symptomatic.16,25,27-38 Only clear concordance of an individual patient’s pain syndrome and imaging findings can suggest causation. Imaging cannot prove causation. Imaging also suffers from sensitivity shortcomings. It is well documented that neuroclaudicatory pain is exacerbated by extension and axial load. The cross-sectional area of the lumbar and cervical central canal, lateral recesses, and neural foramina are known to decrease with extension and axial load.39 Studies by Danielson and Willem have shown that axial loading and extension will reduce

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Table 43-2  Estimated Accuracy of Imaging Technique for Lumbar Spine Conditions* Technique

Sensitivity

Specificity

Positive Likelihood Ratio

Negative Likelihood Ratio

Cancer

0.6

0.95-0.995

12-120

0.40-0.42

Infection

0.82

0.57

11.9

0.32

Ankylosing spondylitis

0.26-0.45

1

ND

0.55-0.74

Herniated disc

0.62-0.9

0.7-0.87

2.1-6.9

0.11-0.54

Stenosis

.09

0.8-0.96

4.5-22

0.10-0.12

0.83-0.93

0.90-0.97

8.3-31

0.70-0.19

0.92

12

0.04

0.43-0.97

1.1-33

0-0.93

0.72-1.0

3.2-ND

0.10-0.14

Pain Radiography

Computed Tomography

Magnetic Resonance Imaging Cancer Infection

0.96

Ankylosing spondylitis

0.56

Herniated disc

0.6-1.0

Stenosis Radionuclide Scanning Cancer Planar imaging

0.74-0.98

0.64-0.81

3.9

.32

SPECT

0.87-0.99

0.91-0.93

9.7

0.14

Infection

0.90

0.78

4.1

0.13

Ankylosing spondylitis

0.26

1.0

ND

0.74

*Estimated

ranges are derived from multiple studies described in the text. ND, not defined; SPECT, single-photon emission computed tomography.

the cross-sectional dimension of the lumbar dural sac in 56% of asymptomatic persons, but in up to 80% of patients with neuroclaudicatory pain syndromes.40,41 Unfortunately, most advanced imaging occurs with the patient in a supine, psoas relaxed (nonextended) position. This position diminishes imaging sensitivity to dynamic processes in which neural compression and pain are experienced only in specific postures. Upright and seated MRI imaging of the spine is commercially available, but suffers from modest image quality at best, due to the low field strength magnets available in this configuration. This may ultimately prove to be a valuable tool, but current devices excessively compromise image quality, and their cost precludes their use being appropriately limited to a problemsolving application. Multiple imaging modalities can be used to investigate the spine pain patient, from simple radiographs to elegant MRI scans. The efficacy of the several imaging modalities used in evaluating common spine disorders has been summarized by Jarvik and Deyo in Table 43-2.1 The American College of Radiology Appropriateness Criteria grade the utility of these imaging modalities in common clinical scenarios, presented in Table 43-3.42

Radiographs In the setting of clinical red flags suggestive of systemic disease, pain unresponsive to conservative measures, or progressive neurologic deficit, imaging should commence with plain radiographs.11 Radiographs are a modest sensitivity screening tool for sinister processes such as neoplasm, infection, or fracture. They also provide vertebral

enumeration, and allow assessment of sagittal and coronal balance. To provide the physiologic information of balance, radiographs should be obtained while the patient is weight-bearing. Single frontal and lateral views of the lumbar spine are adequate. Spot images of the lumbosacral junction, oblique views, and flexion-extension views should not be obtained on a routine basis. They provide little additional information, and significantly increase radiation exposure.43 The significance of vertebral enumeration should not be underestimated. There are anomalies of segmentation at the lumbosacral junction in 7% to 12% of the back pain population.44 Radiographs should establish the convention of vertebral numbering for all subsequent advanced imaging in the individual patient, preventing wrong level minimally invasive or surgical interventions. Radiographic identification of morphologic changes of disc degeneration or osteoarthritis in lumbar zygapophyseal or sacroiliac joints has no value in identifying the cause of an individual patient’s pain.45 Radiographic manifestations of disc degeneration include loss of disc space height, nitrogen gas within the disc, and end plate hypertrophs; these findings have no predictive value for discogenic pain. Similarly, radiographic findings of osteoarthritis, including hypertrophic change, sclerosis, joint space narrowing, gas within the joint space and subchondral cyst formation do not correlate with response to intraarticular anesthetic injections. Morphologically degenerated joints are most commonly asymptomatic, and joints that appear normal radiographically may be painful. Radiographs provide a modest sensitivity screen for systemic disease causal of back pain, which may require advanced imaging to characterize and establish extent of disease (Fig. 43-1). The most common neoplastic condition is metastatic disease. Skeletal

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43

Table 43-3  Clinical Condition—Low Back Pain MRI (lumbar spine, without ­contrast)

MRI (lumbar spine, ­without and with contrast)

CT (lumbar spine, without ­contrast)

CT (lumbar spine, without and with contrast)

X-ray ­(lumbar spine)

CT Myelogram

Myelogram

Bone scan

Uncomplicated, no “red flags”

2

2

2

N/A

2

2b

2a

2

Low velocity trauma, osteoporosis, and/or age >70

8

3

6b

N/A

6

1c

1b

4

Suspicion of ­cancer, infection or ­immunosuppression

8

7

4

N/A

5

2b

2b

5

Radiculopathy

8

5b

5

N/A

3

5a,b

2e

2

Prior lumbar surgery

8

8c

6b

N/A

5d

5b

2b

5

Cauda equina ­syndrome

8a

8c

N/A

4b,c

3

6a,b

2e

2

Note: Appropriateness criteria scale from 1 to 9, 1, least appropriate; 9, most appropriate; aindicates CT and myelography often combined; buseful if MRI is contraindicated or nondiagnostic; cdifferentiates disk versus scar; dflex/extension may be useful; euse of contrast depends on clinical circumstances.

metastases are primarily blastic (bone forming), lytic (bone destroying), or of mixed type. Radiographs primarily image cortical bone. Metastases most commonly involve trabecular bone; at least 50% of trabecular bone mass must be destroyed to be visible on a radiograph. Radiographs therefore have only modest sensitivity (60%) in the detection of metastatic disease.1 Myeloma may also be initially suggested by radiographic evaluation; myeloma typically manifests as small discrete lytic lesions without sclerotic margination. When diffuse, myeloma may be indistinguishable from metabolic osteoporosis. Primary bone tumors are rare causes of spine-related pain. Osteoid osteoma deserves mention because it commonly presents with nocturnal pain.46 This neoplasm of adolescents and young adults has a posterior element predilection, and it generates a lesion consisting of a central lytic nidus with considerable surrounding sclerotic reaction. The diagnosis is seldom made with plain films; CT imaging, with image directed biopsy and radio frequency ablation constitute standard of care. Osteoid osteomas may also be identified on MRI examinations or bone scans as focal intensely enhancing (or metabolically active) posterior element lesions.47 Radiographs may also suggest infectious or inflammatory disease. Radiographic findings of infectious spondylodiscitis (disc space infection) only become apparent several weeks after the onset of disease.48 Because disc space infection in the adult begins as a hematologically seeded vertebral osteomyelitis, radiographs initially demonstrate rarefaction in the anterior subchondral bone adjacent to the end plates within a single disc space. Over time, there will be frank end-plate destruction with loss of disc space height.48 These findings should provoke an urgent MRI examination with gadolinium enhancement. Granulomatous disease (TB, brucellosis) may be indistinguishable from pyogenic disc space infection. Granulomatous discitis more commonly spares the disc space with vertebral collapse and kyphotic deformity at the site of infection.48 Inflammatory spondyloarthropathies may be suggested or diagnosed with plain radiographs. Rheumatoid arthritis primarily

involves the cervical spine, with inflammatory destruction of the transverse ligament binding the dens to C1 with consequent atlantoaxial subluxation.48 There is frequently multilevel cervical disc space narrowing with low grade anterior subluxations resulting in a stair-step appearance to the cervical spine. The seronegative spondyloarthropathies are more commonly apparent in the sacroiliac joints, lumbar and thoracic regions (Fig. 43-2). Narrowing of the sacroiliac joints with associated indistinct cortical surfaces and adjacent sclerosis may herald ankylosing spondylitis, psoriatic arthritis, or Reiter syndrome. The ankylosing spondylitis patient may also have fusion of portions of the thoracolumbar or cervical spine with vertically oriented, gracile syndesmophytes bridging adjacent vertebral bodies. The long-segment spine rigidity in these patients makes them susceptible to catastrophic fracture dislocation, often with neurologic compromise, even with modest trauma. Such fractures may be difficult to visualize with plain radiographs, and the threshold for use of advanced imaging should be very low in ankylosing spondylitis patients suffering trauma.49 Compression fractures can be identified on plain radiographs, but the acuity of a fracture may not be apparent in the absence of serial images. MRI or technetium bone scan can characterize fractures as acute or subacute, metabolically active, and therefore more likely to respond to bone augmentation procedures such as vertebroplasty (Fig. 43-3). However, recent randomized controlled trials have raised questions regarding the efficacy of vertebroplasty.50,51 ­Similarly, pelvic insufficiency fractures may be apparent on radiographs within the sacral ala, pubic rami, pubic symphysis, and periacetabular regions of the pelvis. The plain film finding of a vertical sclerotic band paralleling the sacroiliac joint in the sacral ala strongly suggests insufficiency fracture. CT, technetium bone scan, or MRI are all more sensitive than radiographs in detection of insufficiency fractures.52,53 Another traumatic entity in which plain films play a role is spondylolysis. Defects in the pars interarticularis may be detected

526  Spine

D

G

C

B

A

E

F

H

Imaging for Chronic Spinal Pain  527 Figure 43-1  Radiographic detection of underlying conditions causal of spine or limb pain. Radiograph (A) and CT image (B) of patient with absent left T12 pedicle, shown to be aneurysmal bone cyst on CT. Radiograph (C) and T1 weighted MRI (D) of patient with spotty demineralization on radiograph, prompting the MRI revealing the innumerable lesions of multiple myeloma. Radiograph (E) and CT (F) of patient with L5 pars defects. Lateral radiograph (G) and CT image (H) of patient with axial pain. Radiograph suggests destruction of the anterior-inferior aspect of L3 body, confirmed on CT with associated paraspinal mass compatible with pyogenic spondylodiscitis.

A

B

C

D

E

Figure 43-2  Ankylosing spondylitis (AS). Pelvic radiograph (A), axial CT (B), and coronal T1 weighted MRI image (C) all show manifestations of AS, with indistinct sacroiliac joints with adjacent sclerosis dominant on the iliac side of the joint. MRI shows patchy mixed signal abnormality about the sacroiliac joints. In another patient, sagittal CT images (D and E) show gracile syndesmophytes bridging the lumbar vertebral bodies. The paramedian image (E) demonstrates fusion of the zygapophyseal joints.

on lateral plain films, with a prevalence of approximately 3% to −10% of the population.54 Most cases are asymptomatic. If pars defects are suspected as the cause of an axial pain syndrome, a localized CT will confirm or refute the presence of such a defect and aid in characterizing the defect as acute or chronic. There is no role for oblique radiographs, which double the gonadal radiation dose over the standard images, and do not advance the diagnosis.43

Computed Tomography Computed tomography has undergone a technologic renaissance in the last decade with the evolution of multidetector scanners. Even the most uncomfortable patient can tolerate the few seconds necessary to obtain a high quality data set, which can then be

43

528  Spine

B

A

C reconstructed in any plane without loss of spatial resolution. CT provides superior imaging of cortical and trabecular bone. It has reasonable contrast resolution, allowing the identification of most root compressive lesions (Fig. 43-4). It is less costly than MRI, more widely available, and is not subject to imaging disqualification due to indwelling magnetically susceptible devices. CT remains inferior to MRI in contrast resolution and cannot identify intrathecal pathology. It is less sensitive than MRI to early inflammatory or infectious processes, and to marrow infiltrative disorders, specifically primary or secondary malignancies. The significant radiation dose incurred by CT must also be weighed in decision making. As with plain radiographs, morphologic changes of disc degeneration, zygapophyseal joint arthrosis and sacroiliac joint osteoarthritis seen on CT do not correlate with pain syndromes, and are of no significance.55,56 Disc herniations are readily identifiable with computed tomography. There is no literature comparing current generation CT scanners with MRI in the detection of

Figure 43-3  Fracture Chronicity. Elderly osteoporotic patient presents with acute axial upper lumbar pain. Radiograph (A) demonstrates compression fractures of L1 and L2 vertebral bodies. No prior films were available to assess chronicity of fractures. On technetium bone scan (B), only the L2 fracture shows increased uptake of tracer. The L2 body was targeted for bone augmentation (C) with good clinical response.

root-compressive lesions. A study by Thornbury in 1993 showed little difference in MRI, CT myelography, or CT alone in detecting root-compressive disease.57 Spine MRI has advanced modestly in the intervening 15 years; CT has been reborn. A more recent study from 2006 showed no evidence that CT is inferior to MRI in detecting disc herniation, although there was more interobserver variability with CT.58 This study used two-slice CT scanners; current scanners in general practice are 64-slice scanners with 128-slice machines being introduced. It can be argued that CT is underused in evaluating the younger patient with root-compressive symptoms and no clinical likelihood of systemic disease. In this setting, CT can provide adequate imaging at a lesser cost than MRI. This is, of course, dependent on the local medical ecosystem; if the patient is a surgical candidate and the surgeon involved demands an MRI for planning purposes, then CT becomes an additive rather than a lower cost substitute test. CT is more sensitive than plain radiographs, but less sensitive than MRI, in the detection of infectious or inflammatory ­spinal lesions.1 Discitis may be suggested when end-plate destructive

Imaging for Chronic Spinal Pain  529

43

A

B

D

E

C

Figure 43-4  CT demonstration of disc herniation. Middle-aged male with acute L3 radicular pain pattern, unable to tolerate MRI. CT images (A, B, and C in descending sequence) well demonstrate the left foraminal disc extrusion displacing the L3 root posteriorly. In another patient, CT images D and E show a large left central and subarticular L5 herniation deforming the thecal sac. There is an associated osseous fragment of end plate accompanying the herniation.

A

B

C

Figure 43-5  CT characterization of pars interarticularis insufficiency fractures. CT image (A) demonstrates sclerosis in the pars interarticularis consistent with stress response and healing potential. CT image (B) shows incomplete pars defects with ill-defined linear lucent zones bilaterally surrounded by modest sclerosis. This lesion also has healing potential. In contrast, CT image (C) is that of a chronic insufficiency fracture with a broad well-defined lucent zone. There may be dense marginal sclerosis. This appearance lacks healing potential.

changes are seen, often accompanied by a paraspinal inflammatory mass.59 CT alone may be insufficient to assess central canal compromise, and CT myelography or MRI may be necessary to assess the need for surgical intervention. Noninfectious inflammatory spondyloarthropathies are more conspicuous on CT than on plain films.60 Like radiographs, however, CT is limited to displaying static morphology and cannot assess physiologic inflammation.

Traumatic or insufficiency fractures are more apparent on CT than on radiographs, particularly with the assistance of multiplanar reconstructions. Assessment of fracture acuity with CT requires evaluation of the fracture line and fragments. Very angular fracture lines and fragments with no marginal sclerosis suggest acuity, whereas smooth remodeling of bone implies chronicity. MRI or technetium bone scans provide more specific, physiologic

530  Spine

assessment of fracture acuity. When fatigue fractures of the pars interarticularis are suspected on plain radiographs, CT can assist in further characterization of the fractures and the prognosis for healing (Fig. 43-5). If sclerosis is present within the pars without a discrete defect, this represents a stress reaction with healing potential. An ill-defined lucent zone with marginal sclerosis is an incomplete fracture—also with healing potential.61 A chronic defect with welldefined rounded and sclerotic margins has no healing potential. The combination of SPECT technetium scan with CT is generally considered the standard of care for complete characterization and treatment planning of spondylotic defects.61 Bony destruction or blastic response as a manifestation of tumor is much more evident on CT than on radiographs; MRI, however, is even more sensitive.1 CT exceeds MRI in its ability to assess the degree of structural compromise caused by neoplastic spinal involvement and, therefore, is critical in determining if surgical stabilization is necessary. Neoplasms that infiltrate marrow without trabecular or cortical destruction, such as lymphoma, may be difficult to identify with CT alone. Neoplastic soft tissue lesions involving the central canal or paraspinal regions may be detected by CT, but will be far more conspicuous on MRI.

CT Myelography The demise of CT myelography has been predicted for more than 2 decades; it nonetheless remains a viable imaging adjunct with a problem-solving role in the lumbar region and a dominant role in

A

D

the cervical spine (Fig. 43-6).48 The addition of radio-opaque contrast material to the subarachnoid space allows detection of subtle epidural lesions of benign or malignant etiology, which encroach on the thecal sac and root sleeves. Intrathecal lesions may also be identified, although they are less well characterized than with MRI. The spatial resolution of CT myelography exceeds that of MRI, a critical parameter in the tight confines of the cervical spine. CT myelography excels at the discrimination between soft disc and bony osteophyte, which may alter the surgical approach in the cervical spine. Myelography is minimally invasive, and it adds considerable cost above CT alone.

MRI MRI remains the preeminent spine imaging modality, a status it has enjoyed over much of the last 2 decades, owing to its superior contrast resolution. MRI remains unchallenged in its ability to discriminate between soft tissues of varying character. Alterations of disc contour (herniations) are evaluated with substantial interobserver reliability.62 Lesions compressing the thecal sac, root sleeves, and exiting nerve roots can be directly visualized and the crosssectional dimension of the thecal sac can be quantified without invasion. Interobserver reliability for these parameters is moderate.63 The soft tissue contrast characteristics of MRI allow detection of neoplastic or inflammatory marrow infiltrative lesions that do not destroy trabecular or cortical bone. MRI is more sensitive than CT or CT myelography in the detection of neoplastic or infectious processes.1 With the use of heavily T2 weighted imaging sequences

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Figure 43-6  CT myelography. T2 weighted MRI image (A) at L4 disc in patient with right L5 radicular pain pattern suggests lateral recess compromise, but is not definitive. Sequential CT myelography images (B) and (C) at L4 disc clearly show effacement of traversing L5 root sleeve by disc herniation. In a patient with left C6 radicular pain, T2 weighted MRI image (D) at C5-6 interspace suggests foraminal narrowing, but cannot determine if this is due to bone or soft disc. CT myelography images (E) and (F) at the C5-6 interspace reveals both soft disc herniation and uncovertebral joint hypertrophy compromising the foramen.

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(short tau inversion recovery, fat-saturated fast spin echo) or contrast enhancement, MRI can image an inflammatory response, allowing potential identification of degenerative or noninfectious inflammatory pain generators.

MRI: Degenerative Disease MRI will identify disc degeneration as loss of the normally high T2 signal in the nuclear compartment of the disc before there is detectable loss of disc space height on either CT or radiographs. This finding alone is not predictive of a painful disc. The disc and the adjacent vertebral cartilaginous end plate are a functional unit; end-plate inflammatory changes (Modic changes) frequently accompany disc degeneration.64 Modic type 1 changes are an inflammatory state

consisting of vascularized granulation tissue within the sub–endplate marrow. MRI demonstrates low T1 signal and high T2 signal with enhancement if gadolinium is administered. Modic 1 change may progress to Modic type 2, in which there is fatty infiltration of sub–end-plate marrow, evidenced by elevated T1 and T2 signal (Fig. 43-7). Immunohistochemistry studies suggest that end-plate abnormalities are related to inflammation and axon growth induced by tumor necrosis factor (TNF); such nerve in-growth in abnormal end plates may be a cause of low back pain.65 This is more prominent in Modic 1 change than Modic 2 change. Modic 3 changes represent sclerosis and are seen as low T1 and low T2 signal on MRI. It is a postinflammatory state.66 Inflammatory end-plate changes have been correlated with a painful disc, with a positive predictive value of 91% in a single small study.67

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Figure 43-7  Modic end-plate changes. Type 1 ­end-plate changes, consisting of vascularized ­granulation tissue, will have diminished T1 signal (A) and elevated T2 signal (B) This imaging finding is associated with the presence of inflammatory mediators in subchondral bone. Type 2 end plate change is fatty infiltration of marrow, likely a less inflammatory state. It is visible as elevated T1  (C) and T2 (D) signal in subchondral bone.

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MRI may also identify annular fissures. As the nuclear-annular junction deteriorates, radial fissures may extend to the outer aspect of the disc annulus. Such fissures, called high intensity zones (HIZs), may be visualized as a focal zone of elevated T2 signal, which may enhance due to the presence of vascularized granulation tissue (Fig. 43-8).68 The initial study showed that an HIZ increases the odds that provocation discography (PD) will be positive in a patient at that level by a factor of 6.5.68 Studies on HIZs since that time have all shown that an HIZ has high specificity (range 0.74 to 0.93)69-73 but variable sensitivity, from as low as 0.0973 to as high as 0.7871 for positive PD. Thus, it is uncommon for an HIZ to occur in a disc that is not painful to PD, and the calculated likelihood ratios (ranging from 1.3 to 6.5 and averaging 4.1) indicate that an HIZ increases the odds that PD will be positive by at least 50%.74 Additionally, although HIZs are present in asymptomatic and symptomatic subjects, they are found significantly more in symptomatic subjects

(prevalence 60% ±15%) than asymptomatic subjects (24% ± 11%).75 The interobserver reliability in identifying a HIZ is fair to good,72,76 with reported kappa values of 0.4476 and 0.57.72 In summary, a “dark disc” on MRI suggests physiologic degeneration but is an imperfect predictor of a painful disc (discogenic pain). The presence of an annular fissure (HIZ) or end-plate inflammatory change (especially Modic 1) enhances the positive predictive value of MRI but still falls short of discography in the identification of a painful disc. Discography also remains controversial as a diagnostic test and is not universally accepted. Attempts to identify a painful disc by imaging ultimately fall prey to the gold standard dilemma—there is no pathologic, surgical, or imaging standard against which measurement can occur. Degenerative discs may undergo herniation, which is the displacement of disc material beyond the normal confines of the intervertebral disc space. The accepted nomenclature for disc herniation

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Figure 43-8  High intensity zone. Focal zone of elevated T2 signal is seen in the L4 posterior annulus on both sagittal (A) and axial (B) images. Note the L4 disc is of generalized low T2 signal and a normal internuclear cleft is not visible. On a fat-saturated T1 weighted postgadolinium image (C), the L4 high-intensity zone enhances, implying it has acquired vascular supply owing to the attempted reparative response.

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Figure 43-9  Herniation nomenclature. Axial plane (A) and sagittal plane (B) illustrations of disc herniation nomenclature. Protrusion and extrusion are shape definitions, but carry the implication that in an extrusion there is complete disruption of the outer annulus.

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has recently been codified (Fig. 43-9).77 Disc herniation by definition involves less than 50% of the circumference of the disc; displacement of greater than 50% of the circumference of the disc may be termed a diffuse bulge. A broad-based herniation encompasses 25% to 50% of disc circumference, whereas a focal herniation involves less than 25% of the disc circumference. Disc herniations may be subdivided into protrusions and extrusions, which are shape definitions but carry implications regarding the integrity of the outer annulus. A protrusion remains bounded by an intact outer annulus; herniated material never exceeds the dimension of the parent disc in any plane (Fig. 43-10). An extrusion is uncontained by an intact annulus and may migrate cephalad or caudal to the disc space level, attaining a dimension greater than the annular defect in the disc from which it originated. A sequestration is a free disc fragment which has lost continuity with its parent disc and undergone migration away from it (Fig. 43-11). The location of herniated disc material in the axial plane may be described as central, subarticular (lateral recess), foraminal, or extraforaminal (far lateral), in progression from the midline laterally. In the patient with radicular pain or radiculopathy, in whom a disc herniation is suspected, imaging should begin with radiographs but may progress to MRI if conservative measures fail and epidural steroid injections or surgical intervention are contemplated.12,15 Ninety percent of lumbar disc herniations occur at the

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L4-5 and L5-S1 interspaces.71 Disc herniations most commonly have a posterolateral vector, impinging on the nerve root (traversing root) which will exit under the next lowest pedicle (L4 disc herniation causing L5 radicular pain syndrome). For a lumbar herniation to affect the like-numbered nerve root, herniated material must migrate cephalad into the neural foramen (Fig. 43-12). In the cervical region, the nerve root exits low in the foramen, directly over the subadjacent pedicle, and is vulnerable to disc herniation from the intervertebral disc at the same level as its exit. Remembering that in the cervical spine the numbering of the exiting root matches the subadjacent vertebral body, most cervical herniations will affect the next lower numbered root (e.g., disc herniation at the C6-7 interspace will affect the exiting C7 root [Fig. 43-13]). Herniations are most evident on T2 weighted images, where the mass effect of the herniation can be directly visualized on the thecal sac or nerve root. The herniated disc material is often of higher T2 signal than the parent disc from which it arose. The imaging natural history of disc herniation in both the lumbar and cervical regions is resolution. Numerous longitudinal imaging studies demonstrate that most disc herniations resolve spontaneously, with larger herniations and extrusions most likely to undergo resorption.78-80 The functional disability incurred by disc herniations is better predicted by psychosocial factors than the size or imaging characteristics of the herniation.81

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Figure 43-10  Disc protrusion. Sagittal T2 weighted MRI image (A) and consecutive axial T2 weighted images (B) and (C) demonstrate left L4 central and subarticular disc protrusion impinging on traversing left L5 root. Left L5 radicular pain syndrome treated with left L5 transforaminal epidural steroid injection (D).

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Figure 43-11  Disc extrusion, peripheral enhancement. Patient with left “hip” pain, experienced in inguinal crease and medial thigh. Sagittal T2 weighted MRI image (A) reveals extruded L3 fragment that has migrated cephalad into left L3 root axilla, confirmed on axial T2 (B) and T1 (C) images. Postcontrast fat-saturated T1 sagittal (D) and (E) axial images show the intense inflammatory epidural enhancement about the disc fragment. The disc material itself does not enhance.

Gadolinium is not typically used in the nonoperated cervical or lumbar spine; when used, it will often show that the volume of herniated disc material (which does not enhance) is relatively small compared to accompanying enhancing granulation tissue. In the postoperative spine, contrast enhancement is mandatory. Imaging is essentially blind to the detection of recurrent disc herniation in the 6 weeks immediately following surgical intervention. Beyond this perioperative period, the use of gadolinium enhancement should allow accuracy of up to 96% in distinguishing recurrent herniation from epidural fibrosis (scar).82,83 Epidural fibrosis enhances uniformly and rapidly following gadolinium administration, whereas herniated disc material enhances minimally and slowly (Fig. 43-14). Extensive epidural fibrosis is in itself a negative prognostic sign in the postoperative patient and is associated with an increased incidence of persistent postoperative radiculopathy.84

In the postoperative setting, the thecal sac should also be examined for evidence of arachnoiditis, usually attributed to hemorrhage within the thecal sac. In this condition, the roots of the cauda equina either clump or are adherent to the neural tube (Fig. 43-15). The dural tube may appear empty of roots which are smoothly scarred to its wall. Clumped roots in arachnoiditis may exhibit enhancement. In severe cases, the subarachnoid space is completely obliterated by scarring. Spinal stenosis describes a clinical syndrome characterized by neurogenic claudication with exertion. Imaging identifies the morphologic substrate of central canal narrowing. Patients who exhibit a narrowed central canal on imaging frequently are asymptomatic and cannot carry the diagnosis of spinal stenosis. Central canal compromise is well displayed on T2 weighted MRI (Fig. 43-16), although CT can also make this diagnosis; CT myelography provides the best spatial resolution in this regard. Central canal narrowing in the lumbar

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Figure 43-12  Foraminal (lateral) disc extrusion. Patient with left L4 radicular pain pattern. Sagittal T1 (A) and T2 (B) weighted MRI images show foraminal disc extrusion. Note that on the T2 weighted image (B) the extruded fragment is of higher T2 signal than the parent disc. The exiting L4 root is displaced laterally on the axial T2 weighted image (C). Epidural contrast injection preceding steroid injection (D) and (E) outlines the disc herniation.

region is usually primarily the result of posterior element impingement: central buckling of the ligamentum flavum, zygapophyseal joint arthropathy, and synovial cysts. Disc herniation and discosteophyte complexes may also contribute from the ventral aspect of the canal. Sagittal T2 weighted MRI or CT myelography images also often demonstrate serpiginous redundant nerve roots or dilated veins within the subarachnoid space in the stenotic central canal. Multilevel central canal stenosis is more likely to provoke clinical symptoms. It must be remembered that advanced imaging obtained on a recumbent patient may be insensitive to dynamic lesions.40 MRI, like radiographs and CT, can identify the morphologic features of zygapophyseal joint osteoarthritis, which have no predictive value for pain generation.56 MRI can, however, also identify inflammatory change using heavily T2 weighted imaging sequences such as short tau inversion recovery (STIR) or fat saturated fast spin

echo. In these sequences, T2 signal abnormality is white against a dark background and is highly conspicuous (Fig. 43-17). Gadolinium enhancement, best seen with fat saturated sequences, is equivalent in its identification of inflammation, but more costly. A recent paper by Czervionke and associates suggests that such T2 signal abnormality may be useful in identifying painful joints.85 This paradigm may apply to the sacroiliac joint as well, although published work to date describes such MRI findings in inflammatory spondyloarthropathy such as ankylosing spondylitis rather than osteoarthritis. Synovial cysts, a manifestation of zygapophyseal joint osteoarthritis, may be a cause of radicular pain syndromes and are readily identified on MRI (Fig. 43-18).86 A rent in the fibrous joint capsule allows the synovial membrane and its contained fluid to form a juxtaarticular cyst, most common at the L4 level. Synovial cysts are present in approximately 10% of patients undergoing MRI imaging

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Figure 43-13  Cervical disc extrusions. Patient presents with right C7 radicular pain syndrome. Sagittal T2 weighted images (A) and (B) show congenital fusion of the C5-6 bodies. Disc extrusion at C6 interspace. Consecutive T2 weighted axial images (C, D, E) at C6-7 interspace demonstrate right-sided extrusion deforming exiting C7 root and mildly deforming cord caudal to root entry zone.

for lumbar pain issues; most of the cysts are dorsal, arising from the inferior recess of the joint and project harmlessly into the multifidus musculature.87 Cysts, which project ventrally into the spinal canal, have a prevalence of slightly greater than 2% and may compress neural elements in the central canal, lateral recess, or neural foramen.86 On MRI, synovial cysts may signal as CSF does, or be heterogeneous owing to hemorrhage or inspissated proteinaceous material. Ultimately, synovial cysts may calcify. If the cyst wall is very thin, this suggests the cyst may collapse with aspiration under image guidance; cysts with a thick fibrous wall of low T2 signal are less amenable to minimally invasive treatment.

MRI: Systemic Disease MRI is the most sensitive modality for the detection of systemic disease, which presents as back or leg pain. This broadly consists of infection, unsuspected trauma, or neoplasm. As noted previously, MRI has superior sensitivity in the early detection of pyogenic or

granulomatous spondylitis.59,88-90 Early MRI findings consist of marrow edema (low T1 signal, high T2 signal) about a disc which will likely have zones of elevated T2 signal within it. Gadolinium administration is essential in cases of spondylodiscitis; it will typically reveal enhancement both within the index disc and its adjacent vertebral bodies as well as in the epidural space and paraspinal soft tissues (Fig. 43-19).59,88 The combination of gallium and technetium nuclear medicine studies has a sensitivity equal to that of MRI in the detection of spondylodiscitis, but will not provide the anatomic information necessary to make a clinical decision regarding medical versus surgical therapy.91 The presence of an epidural abscess in the setting of neurologic compromise may provoke emergent surgical decompression. Only MRI can provide this anatomic information, as well as provide high sensitivity in the detection of less fulminant cases of spondylodiscitis.59,88 The imaging appearance of discitis on MRI lags behind the clinical state. Imaging findings may continue to be dramatic when the patient has clearly demonstrated clinical response to therapy. In the author’s clinical experience, therapy should be followed

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Figure 43-14  Recurrent disc herniation. Patient with history of left L5 discectomy presents with new left S1 radicular pain. T2 weighted sagittal (A) and axial (B) MRI images reveal apparent left L5 disc extrusion. In the postoperative setting, this cannot be known without use of gadolinium contrast material. Pre- (C) and postgadolinium (D) T1 weighted axial images demonstrate multiple extruded fragments, which do not enhance, separated by thin enhancing septa of granulation tissue. The left S1 root sleeve is effaced.

with biochemical markers such as C-reactive protein, not MRI; repeat imaging should be reserved for situations where there is concern for failure of therapy and compromise of the central spinal canal. Granulomatous spondylodiscitis may be indistinguishable from pyogenic disease, but is more likely to spare the disc with vertebral collapse and kyphotic deformity (Fig. 43-20).48 Up to 50% of cases of granulomatous spondylitis have no disc space involvement, and the isolated vertebral lesions can mimic metastatic disease.92 CT may provide a clue to the infectious origin of such lesions by demonstrating a broad sclerotic margin about the lytic lesions, implying a more indolent course then is seen with most neoplasms. Diagnosis frequently depends on image-guided biopsy and culture. Assay for tuberculous RNA can provide rapid (24 hour) diagnosis of tuberculous infection while awaiting cultures to provide sensitivity information. MRI can detect the characteristic inflammatory response about the sacroiliac joints in the seronegative spondyloarthropathies before morphologic changes are detectable on radiographs or CT. Technetium bone scan is equally sensitive in this regard. In rheumatoid arthritis, MRI can directly evaluate the integrity of the transverse ligament at C1-2, the presence of pannus formation, and potential compromise of the cervical spinal canal.48 MRI is not typically used in the acute traumatic setting, but has a role in evaluation of traumatic lesions as subacute and chronic

pain generators. Osteoporotic compression fractures are a relatively common cause of back pain in the elderly.1 Many patients respond well to analgesics and perhaps bracing. Vertebroplasty has been shown to be no better than placebo,50,51 and although these fractures can be severely painful initially, the natural history is relatively good.93 Unfortunately, a small percentage of vertebral compression fractures are the result of metastatic disease or hematologic malignancy; vertebral body expansion with associated paraspinal or epidural enhancing mass suggests neoplasm. Image guided biopsy can then establish a diagnosis. Insufficiency fractures are also common in the pelvis, most often seen in the sacrum (Fig. 43-21) but also in the pubic rami, body of the pubic bone, or periacetabular regions. Linear zones of elevated T2 signal or diminished T1 signal in characteristic locations (Honda sign in sacral lesions) suggest insufficiency fracture; MRI signal abnormality will be apparent before reactive sclerosis is detectable by CT or radiographs.94 Technetium bone scan is similar in sensitivity to MRI for insufficiency fracture detection.95,96 Neoplasm, whether extradural or intradural, is best detected and characterized by MRI.1 Most extradural lesions will be metastases and manifest as vertebral lesions with low T1, high T2 signal enhancement with gadolinium, perhaps with extension into the

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Figure 43-15  Arachnoiditis. T2 weighted MRI images show a normal distribution of roots in the dorsal thecal sac in the upper lumbar region (A), but thickened, clumped roots in the lower lumbar canal (B and C). In another patient, there is a paucity of roots evident in the thecal sac on a sagittal T2 image (D). Axial images in the lower lumbar region (E and F) reveal that all lumbar roots are adherent to the dural tube, giving the impression of an “empty sac.”

epidural space. Hematologic malignancies may diffusely replace marrow fat, with uniformly low T1 signal that may not be readily apparent; marrow should always be brighter than disc on T1 images. Intradural lesions include meningiomas, schwannomas, leptomeningeal metastases; the intramedullary neoplasms include ependymoma, astrocytoma, and hemangioblastoma. These will be detected as enhancing mass lesions.

Nuclear Medicine Nuclear medicine techniques, including technetium bone scans, gallium scanning, and positron emission tomography (PET) hold niche roles in evaluating the patient with pain of spinal origin. With the addition of single photon emission computed tomography (SPECT), technetium bone scanning acquires greater sensitivity and significantly improved anatomic resolution. By imaging metabolic activity (bone turnover), technetium scans are sensitive, but relatively nonspecific, in the detection of inflammatory, infectious, traumatic, and neoplastic lesions. In degenerative disease, the presence of increased activity on a bone scan may identify active inflammation in zygapophyseal and sacroiliac joints, providing a target for minimally invasive intervention. It is questionable whether it is

efficacious in terms of cost or radiation dose to use bone scanning as an additive test for such purposes. Characterization of compression fractures in terms of chronicity can be readily accomplished by bone scan; this is particularly useful in the non–MRI-compatible patient. Bone scanning is highly sensitive in the detection of insufficiency fractures of the pelvis. Technetium scans also play a role in the detection of spondylolysis; the presence of increased activity in a pars interarticularis implies an actively metabolic lesion, a likely source of pain (Fig. 43-22).61 Limited CT may be necessary for further characterization of healing potential and therapy planning. SPECT bone scans are very useful in the detection of pseudarthroses in patients who present with pain following fusion surgery.97 The combination of gallium plus technetium scans is highly sensitive and specific for the detection of spine infection.98 It suffers from its lack of anatomic information, which will likely be necessary for planning therapy and result in additive tests; MRI is generally preferred when spine infection is suspected. Technetium scanning room retains its longstanding role in assessing tumor burden. The assessment of tumor burden is now being assumed by PET scanning. Integrated PET/CT scanners provide metabolic and anatomic information, hopefully obviating the need for additional imaging in following the patient with neoplastic disease.

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Figure 43-16  Central canal stenosis. Patient with pseudoclaudicatory pain syndrome exhibits multilevel central canal compromise on sagittal T2 MRI image (A). Stenosis is moderate at L3 interspace (B), severe at L4 interspace level (C), with a widely patent central canal at L2 (D). In another patient with central canal compromise due to epidural lipomatosis, the prominent ventral, dorsal, and lateral epidural fat is well displayed on T1 weighted sagittal (E) and axial (F) and (G) images.

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Figure 43-17  Zygapophyseal joint. Radiograph (A) in patient with right-sided axial pain shows sclerosis in right L2-3 joint at junctional scoliotic curve above fusion construct. The morphologic change alone does not correlate with a painful joint. Increased uptake on technetium bone scan (B) at this joint does predict favorable response to intervention. In a different patient, severe structural change of osteoarthritis on CT scan(C) at L4-5 joint is not, itself, predictive of pain generation. Enhancement in and about this joint on fat-saturated T1 weighted MRI images (D) and (E) is predictive of a pain generator.

Imaging Principles and Strategies The foregoing discussion of the literature which bears on imaging efficacy, sensitivity, and specificity shortcomings of all spine imaging and the characteristics of multiple imaging modalities may be distilled into the following basic imaging principles and strategies: 1. A  ll imaging modalities suffer from a significant lack of specificity. There is a large burden of asymptomatic degenerative phenomenon seen on all imaging studies, whose prevalence increases with patient age. 2. A  dvanced imaging is typically performed without axial load or postural extension, which may make it insensitive to dynamic lesions. 3. A  lthough spine imaging can provide benefit by identifying underlying systemic disease or planning interventions in

degenerative conditions, its risks must be considered, including financial cost, radiation exposure, labeling the patient as suffering from a degenerative disorder, or provoking unwarranted interventions. 4. Th  ere is no role for imaging at the acute presentation of the patient with back, neck, or limb pain in the absence of red flag features suggesting underlying systemic disease or progressive neurologic deficit. 5. W  hen imaging commences, it should be performed with weight-bearing radiographs, which will establish vertebral enumeration, assess sagittal and coronal balance, and provide a low sensitivity screen for underlying systemic disease. 6. I n the patient with a progressive neurologic deficit or unremitting pain and a history suggestive of disc herniation, MRI is the imaging modality of choice to guide minimally invasive intervention or plan surgical therapy. In the MRI-incompatible

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Figure 43-18  Synovial cyst. Patient presented in 2003 with right L5 radicular pain syndrome. T2 weighted MRI images (A) and (B) show synovial cyst arising from right L4-5 zygapophyseal joint deforming thecal sac, impinging on traversing right L5 root. Right L5 transforaminal epidural steroid injection (C) combined with intraarticular administration of betamethasone (D) provided durable pain relief. The same patient presented in 2007 with new axial lumbar pain. T2 weighted MRI images (E and F) show new L5 compression fracture; the synovial cyst is no longer present.

patient, or the patient unable to tolerate a prolonged examination, CT provides a rapid, lower-cost alternative. 7. I n the cervical spine, CT myelography retains a role as an operative planning study owing to its superior spatial resolution and ability to discriminate between bony or soft tissue neural compromise. 8. Th  e imaging natural history of disc herniation is resolution. Large volume herniations and extrusions are most likely to resolve. There is very poor correlation between the perceived “severity” of the imaging finding and the intensity of pain or dysfunction experienced by the patient. Psychosocial factors are the primary determinants of functional disability. 9. I n patients with red flag features concerning for systemic disease, MRI is the imaging test of choice and gadolinium enhancement should be considered. Ideally, if the imaging is monitored in real time by a radiologist, a decision can be made at that time whether to add the cost and imaging time associated with contrast use.

10. M  orphologic features of osteoarthritis identified on radiographs, CT, or MRI have no predictive value in identifying pain generators. 11. I maging evidence of inflammation, including elevated T2 signal or enhancement on MRI, or increased metabolic activity on technetium bone scans, may identify degenerative pain generators. A heavily T2 weighted imaging sequence (STIR, fat suppressed FSE) should be included on MRI imaging studies performed to investigate unexplained pain. 12) M  ost importantly, treat the patient, do not treat imaging findings. The best understanding of the relevance of imaging findings will occur when there is close communication between the spine clinician and the imaging professional, and their skill sets overlap. The spine clinician must understand the physical principles underlying imaging and its inherent strengths and weaknesses. The imaging professional must be knowledgeable of clinical pain syndromes, their pathophysiology, and imaging manifestations.

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Figure 43-19  Pyogenic spondylodiscitis. Patient presents with axial neck pain, myelopathy. Sagittal T1(A) and T2 (B) weighted MRI images demonstrate diminished T1 signal in the C3 and C4 vertebral bodies, narrowed C3 disc space and ventral epidural tissue deforming the cord. Fat-saturated postgadolinium sagittal (C) and axial (D) T1 images show enhancement in the C3 and C4 bodies, ventral epidural space, C3 disc space, and prevertebral tissue consistent with pyogenic spondylodiscitis. Small ventral epidural abscess is present to the right of midline on axial image (D).

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Figure 43-20  Granulomatous spondylodiscitis (Mycobacterium tuberculosis). Young female with axial thoracolumbar junction pain. Vertebral body and disc space destruction with kyphotic deformity is demonstrated on sagittal T2 weighted MRI (A). Coronal (B) and axial (C) postgadolinium T1 weighted images reveal extensive paraspinal abscesses, vertebral body destruction, and epidural abscess. Patient responded well to medical therapy and did not require surgical ­débridement. A second patient presented with L5 radicular pain. Fat-saturated sagittal T2 image (D) shows multiple vertebral body and posterior element lesions; discs are spared. Epidural disease is present at L5 level. CT images at T10 (E) and L4 (F) show destructive vertebral lesions extending into paraspinal tissues. Imaging had suggested metastatic disease. Note, however, the sclerotic bony reaction suggesting indolent lesions. Biopsy revealed M. tuberculosis.

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Figure 43-21  Insufficiency fracture. Elderly female with axial pelvic pain. T1 weighted coronal MRI images (A and B) show linear low signal medial to sacroiliac joints. Coronal fat-saturated T2 weighted MRI images (C) and (D) show ­vertically oriented band of high signal in the sacral ala jointed by a horizontal band traversing S1 segment, completing the “H” or Honda sign. (Imagination helps.)

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Figure 43-22  Imaging of spondylolysis. Fourteen-year-old female volleyball player complains of left-sided low lumbar axial pain. Lateral radiograph (A) is unremarkable. Planar images from technetium bone scan (B) suggest increased uptake in left L5 posterior elements. SPECT images (C) confirm foc al uptake in region of left L5 pars interarticularis. Sagittal reconstruction of limited CT demonstrates subtle lucent line traversing left L5 pars (D). Patient responded well to conservative care.

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REFERENCES   1. Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med. 2002;137:586-597.   2. Deyo RA, Mirza SK, Martin BI. Back pain prevalence and visit rates: estimates from U.S. national surveys. Spine. 2002;2006;31:2724-2727.   3. Coste J, Delecoeuillerie G, Cohen de Lara A, et al. Clinical course and prognostic factors in acute low back pain: an inception cohort study in primary care practice. BMJ. 1994;308:577-580.   4. Von Korff M, Deyo RA, Cherkin D, et al. Back pain in primary care. Outcomes at 1 year. Spine. 1993;18:855-862.   5. Croft PR, Macfarlane GJ, Papageorgiou AC, et al. Outcome of low back pain in general practice: a prospective study. BMJ. 1998;316:1356-1359.   6. van den Hoogen HJ, Koes BW, van Eijk JT, et al. On the course of low back pain in general practice: a one year follow up study. Ann Rheum Dis. 1998;57:13-19.   7. McGuirk B, King W, Govind J, et al. Safety, efficacy, and cost effectiveness of evidence-based guidelines for the management of acute low back pain in primary care. Spine. 2001;26:2615-2622.   8. Deyo RA, Mirza SK, Turner JA, et al. Overtreating chronic back pain: time to back off? J Am Board Fam Med. 2009;22:62-68.   9. Chou R, Fu R, Carrino JA, et al. Imaging strategies for low-back pain: systematic review and meta-analysis. Lancet. 2009;373:463-472. 10. Carragee E, Alamin T, Cheng I, et al. Are first-time episodes of serious LBP associated with new MRI findings? Spine J. 2006;6:624-635. 11. Davis PC, Wippold II FJ, Brunberg JA, et al. Expert Panel on Neurologic Imaging. ACR Appropriateness Criteria® low back pain. Reston, Va: American College of Radiology (ACR); 2008. 12. Bradley Jr WG. Low back pain. AJNR Am J Neuroradiol. 2007;28:990-992. 13. Acute low back problems in adults: assessment and treatment. Agency for Health Care Policy and Research. Clin Pract Guidel Quick Ref Guide Clin. 1994:iii-25. 14. Evidence-based Management of Acute Musculoskeletal Pain: NHMRC (Australian Government); 2003. 15. Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007;147:478-491. 16. Jarvik JG, Hollingworth W, Heagerty PJ, et al. Three-year incidence of low back pain in an initially asymptomatic cohort: clinical and imaging risk factors. Spine. 2005;30:1541-1548. 17. Engers A, Jellema P, Wensing M, et al. Individual patient education for low back pain. Cochrane Database of Syst Rev. 2008: CD004057. 18. Buchbinder R. Self-management education en masse: effectiveness of the Back Pain: Don’t Take It Lying Down mass media campaign. Med J Aust. 2008;189:S29-S32. 19. Mettler Jr FA, Huda W, Yoshizumi TT, Mahesh M. Effective doses in radiology and diagnostic nuclear medicine: a catalog. Radiology. 2008;248:254-263. 20. Maniadakis N, Gray A. The economic burden of back pain in the UK. Pain. 2000;84:95-103. 21. Centres for Medicare & Medicaid Services. [http://www.cms.hhs.gov/]. 2009. 22. Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic resonance imaging vs. radiographs for patients with low back pain: a randomized controlled trial. JAMA. 2003;289:2810-2818. 23. Lurie JD, Birkmeyer NJ, Weinstein JN. Rates of advanced spinal imaging and spine surgery. Spine. 2003;28:616-620. 24. Hitselberger WE, Witten RM. Abnormal myelograms in asymptomatic patients. J Neurosurg. 1968;28:204-206. 25. Wiesel SW, Tsourmas N, Feffer HL, et al. A study of computer-assisted tomography. I. The incidence of positive CAT scans in an asymptomatic group of patients. Spine. 1984;9:549-551. 26. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am. 1990;72:403-408.

27. Boden SD, McCowin PR, Davis DO, et al. Abnormal magnetic-resonance scans of the cervical spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am. 1990;72:1178-1184. 28. Alyas F, Turner M, Connell D. MRI findings in the lumbar spines of asymptomatic, adolescent, elite tennis players. Br J Sports Med. 2007;41:836-841. 29. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med. 1994;331:69-73. 30. Boos N, Rieder R, Schade V, et al. 1995 Volvo Award in clinical sciences. The diagnostic accuracy of magnetic resonance imaging, work perception, and psychosocial factors in identifying symptomatic disc herniations. Spine. 1995;20:2613-2625. 31. Jarvik JJ, Hollingworth W, Heagerty P, et al. The Longitudinal Assessment of Imaging and Disability of the Back (LAIDBack) Study: baseline data. Spine. 2001;26:1158-1166. 32. Hellstrom M, Jacobsson B, Sward L, Peterson L. Radiologic abnormalities of the thoraco-lumbar spine in athletes. Acta Radiol. 1990;31:127-132. 33. Weinreb JC, Wolbarsht LB, Cohen JM, et al. Prevalence of lumbosacral intervertebral disk abnormalities on MR images in pregnant and asymptomatic nonpregnant women. Radiology. 1989;170:125-128. 34. Burns JW, Loecker TH, Fischer Jr JR, et al. Prevalence and significance of spinal disc abnormalities in an asymptomatic acceleration subject panel. Aviat Space Environ Med. 1996;67:849-853. 35. Stadnik TW, Lee RR, Coen HL, et al. Annular tears and disk herniation: prevalence and contrast enhancement on MR images in the absence of low back pain or sciatica. Radiology. 1998;206:49-55. 36. Weishaupt D, Zanetti M, Hodler J, Boos N. MR imaging of the lumbar spine: prevalence of intervertebral disk extrusion and sequestration, nerve root compression, end plate abnormalities, and osteoarthritis of the facet joints in asymptomatic volunteers. Radiology. 1998;209:661-666. 37. Carragee EJ, Paragioudakis SJ, Khurana S. 2000 Volvo Award winner in clinical studies: Lumbar high-intensity zone and discography in subjects without low back problems. Spine. 2000;25:2987-2992. 38. Chung CB, Vande Berg BC, Tavernier T, et al. End plate marrow changes in the asymptomatic lumbosacral spine: frequency, distribution and correlation with age and degenerative changes. Skeletal Radiol. 2004;33:399-404. 39. Schmid MR, Stucki G, Duewell S, et al. Changes in cross-sectional measurements of the spinal canal and intervertebral foramina as a function of body position: in vivo studies on an open-configuration MR system. AJR Am J Roentgenol. 1999;172:1095-1102. 40. Danielson B, Willén J. Axially loaded magnetic resonance image of the lumbar spine in asymptomatic individuals. Spine. 2001;26: 2601-2606. 41. Willen J, Danielson B, Gaulitz A, et al. Dynamic effects on the lumbar spinal canal: axially loaded CT-myelography and MRI in patients with sciatica and/or neurogenic claudication. Spine. 1997;22:2968-2976. 42. Davis PC, Wippold II FJ, Brunberg JA, et al. Expert Panel on Neurologic Imaging. ACR Appropriateness Criteria® low back pain. Reston, Va: American College of Radiology (ACR); 2008. 43. Hall FM. Back pain and the radiologist. Radiology. 1980;137:861-863. 44. Elster AD. Bertolotti’s syndrome revisited. Transitional vertebrae of the lumbar spine. Spine. 1989;14:1373-1377. 45. Schwarzer AC, Derby R, Aprill CN, et al. The value of the provocation response in lumbar zygapophyseal joint injections. Clin J Pain. 1994;10:309-313. 46. Resnick D, Kyriakos M, Greenway G. Tumors and tumor-like lesions of bone. Diagnosis of Bone and Joint Disorders. 3rd ed. Philadelphia: WB Saunders; 1995:3363-3369. 47. Davies M, Cassar-Pullicino VN, Davies AM, et al. The diagnostic accuracy of MR imaging in osteoid osteoma. Skeletal Radiol. 2002;31:559-569.

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546  Spine 48. Ross JS, Brant-Zawadzki M, Moore KR, et al. Diagnostic Imaging. Spine Salt Lake City, UT: Amirsys; 2007. 49. Fordham S, Lloyd G. Clinical management of injured patients with ankylosing spondylitis. BMJ. 2009;339:b2568. 50. Kallmes DF, Comstock BA, Heagerty PJ, et al. A randomized trial of vertebroplasty for osteoporotic spinal fractures. N Engl J Med. 2009;361:569-579. 51. Buchbinder R, Osborne RH, Ebeling PR, et al. A randomized trial of vertebroplasty for painful osteoporotic vertebral fractures. N Engl J Med. 2009;361:557-568. 52. Grangier C, Garcia J, Howarth NR, et al. Role of MRI in the diagnosis of insufficiency fractures of the sacrum and acetabular roof. Skeletal Radiol. 1997;26:517-524. 53. Fujii M, Abe K, Hayashi K, et al. Honda sign and variants in patients suspected of having a sacral insufficiency fracture. Clin Nucl Med. 2005;30:165-169. 54. Belfi LM, Ortiz AO, Katz DS. Computed tomography evaluation of spondylolysis and spondylolisthesis in asymptomatic patients. Spine. 2006;31:E907-E910. 55. Schwarzer AC, Wang SC, O’Driscoll D, et al. The ability of computed tomography to identify a painful zygapophysial joint in patients with chronic low back pain. Spine. 1995;20:907-912. 56. Elgafy H, Semaan HB, Ebraheim NA, Coombs RJ. Computed tomography findings in patients with sacroiliac pain. Clin Orthop Relat Res. 2001:112-118. 57. Thornbury JR, Fryback DG, Turski PA, et al. Disk-caused nerve compression in patients with acute low-back pain: diagnosis with MR, CT myelography, and plain CT. Radiology. 1993;186:731-738. 58. van Rijn JC, Klemetso N, Reitsma JB, et al. Observer variation in the evaluation of lumbar herniated discs and root compression: Spiral CT compared with MRI. Br J Radiol. 2006;79:372-377. 59. Maiuri F, Iaconetta G, Gallicchio B, et al. Spondylodiscitis. Clinical and magnetic resonance diagnosis. Spine. 1997;22:1741-1746. 60. Bennett DL, Ohashi K, el-Khoury GY. Spondyloarthropathies: ankylosing spondylitis and psoriatic arthritis. Radiol Clin North Am. 2004;42:121-134. 61. Gregory PL, Batt ME, Kerslake RW, et al. The value of combining single photon emission computerised tomography and computerised tomography in the investigation of spondylolysis. Eur Spine J. 2004;13:503-509. 62. Lurie JD, Tosteson AN, Tosteson TD, et al. Reliability of magnetic resonance imaging readings for lumbar disc herniation in the Spine Patient Outcomes Research Trial (SPORT). Spine. 2008;33:991-998. 63. Ohtori S, Inoue G, Ito T, et al. Tumor necrosis factor-immunoreactive cells and PGP 9.5-immunoreactive nerve fibers in vertebral endplates of patients with discogenic low back pain and Modic Type 1 or Type 2 changes on MRI. Spine. 2006;31:1026-1031. 64. Modic MT, Steinberg PM, Ross JS, et al. Degenerative disk disease: assessment of changes in vertebral body marrow with MR imaging. Radiology. 1988;166:193-199. 65. Ohtori S, Inoue G, Ito T, et al. Tumor necrosis factor-immunoreactive cells and PGP 9.5-immunoreactive nerve fibers in vertebral endplates of patients with discogenic low back pain and modic type 1 or type 2 changes on MRI. Spine. 2006;31:1026-1031:(Phila Pa 1976.). 66. Modic MT, Steinberg PM, Ross JS, et al. Degenerative disk disease: Assessment of changes in vertebral body marrow with MR imaging. Radiology. 1988;166:193-199. 67. Braithwaite I, White J, Saifuddin A, et al. Vertebral end-plate (Modic) changes on lumbar spine MRI: correlation with pain reproduction at lumbar discography. Eur Spine J. 1998;7:363-368. 68. Aprill C, Bogduk N. High-intensity zone: a diagnostic sign of ­painful lumbar disc on magnetic resonance imaging. Br J Radiol. 1992;65: 361-369. 69. Ito M, Incorvaia KM, Fredrickson BE, et al. Predictive signs of discogenic lumbar pain on magnetic resonance imaging with discography correlation. Spine. 1998;23:1252-1260.

70. Saifuddin A, Braithwaite I, White J, et al. The value of lumbar spine magnetic resonance imaging in the demonstration of anular tears. Spine. 1998;23:453-457. 71. Schellhas KP, Pollei SR, Gundry CR, Heithoff KB. Lumbar disc highintensity zone. Correlation of magnetic resonance imaging and discography. Spine. 1996;21:79-86. 72. Smith BM, Hurwitz EL, Solsberg D, et al. Interobserver reliability of detecting lumbar intervertebral disc high-intensity zone on magnetic resonance imaging and association of high-intensity zone with pain and anular disruption. Spine. 1998;23:2074-2080. 73. Ricketson R, Simmons JW, Hauser BO. The prolapsed intervertebral disc. The high-intensity zone with discography correlation. Spine. 1996;21:2758-2762. 74. Bogduk N. Why I pursue discogenic pain: Annual Scientific Meeting of the German Pain Society; 2010, 20-10-2005. 75. Carragee EJ, Paragioudakis SJ, Khurana S. 2000 Volvo Award winner in clinical studies: Lumbar high-intensity zone and discography in subjects without low back problems. Spine. 2000;25:2987-2992. 76. Carrino JA, Lurie JD, Tosteson AN, et al. Lumbar spine: reliability of MR imaging findings. Radiology. 2009;250:161-170. 77. Fardon DF, Milette PC. Nomenclature and classification of lumbar disc pathology. Recommendations of the Combined task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine. 2001;26:E93-E113. 78. Teplick JG, Haskin ME. Spontaneous regression of herniated nucleus pulposus. AJR Am J Roentgenol. 1985;145:371-375. 79. Saal JA, Saal JS, Herzog RJ. The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine. 1990;15:683-686. 80. Bush K, Cowan N, Katz DE, Gishen P. The natural history of sciatica associated with disc pathology. A prospective study with clinical and independent radiologic follow-up. Spine. 1992;17:1205-1212. 81. Carragee EJ, Alamin TF, Miller JL, Carragee JM. Discographic, MRI and psychosocial determinants of low back pain disability and remission: a prospective study in subjects with benign persistent back pain. Spine J. 2005;5:24-35. 82. Ross JS, Zepp R, Modic MT. The postoperative lumbar spine: enhanced MR evaluation of the intervertebral disk. AJNR Am J Neuroradiol. 1996;17:323-331. 83. Ross JS. MR imaging of the postoperative lumbar spine. Magn Reson Imaging Clin N Am. 1999;7:513-524. 84. Ross JS, Robertson JT, Frederickson RC, et al. Association between peridural scar and recurrent radicular pain after lumbar discectomy: magnetic resonance evaluation. ADCON-L European Study Group. Neurosurgery. 1996;38:855-861. 85. Czervionke LF, Fenton DS. Fat-saturated MR imaging in the detection of inflammatory facet arthropathy (facet synovitis) in the lumbar spine. Pain Med. 2008;9:400-406. 86. Phuong LK, Atkinson JL, Thielen KR. Far lateral extraforaminal lumbar synovial cyst: report of two cases. Neurosurgery. 2002;51:505-507. 87. Apostolaki E, Davies AM, Evans N, Cassar-Pullicino VN. MR imaging of lumbar facet joint synovial cysts. Eur Radiol. 2000;10:615-623. 88. Modic MT, Feiglin DH, Piraino DW, et al. Vertebral osteomyelitis: assessment using MR. Radiology. 1985;157:157-166. 89. Slipman CW, Shin CH, Patel RK, et al. Etiologies of failed back surgery syndrome. Pain Med. 2002;3:200-214. 90. Perronne C, Saba J, Behloul Z, et al. Pyogenic and tuberculous spondylodiskitis (vertebral osteomyelitis) in 80 adult patients. Clin Infect Dis. 1994;19:746-750. 91. Hadjipavlou AG, Cesani-Vazquez F, Villaneuva-Meyer J. The effectiveness of gallium citrate Ga 67 radionuclide imaging in vertebral osteomyelitis revisited. Am J Orthop. 1998;27:179-183. 92. Whalen JL, Brown ML, McLeod R, Fitzgerald Jr RH. Limitations of indium leukocyte imaging for the diagnosis of spine infections. Spine. 1991;16:193-197. 93. Lyritis GP, Mayasis B, Tsakalakos N, et al. The natural history of the osteoporotic vertebral fracture. Clin Rheumatol. 1989;66-69.

Imaging for Chronic Spinal Pain  547 94. Lourie H. Spontaneous osteoporotic fracture of the sacrum. An unrecognized syndrome of the elderly. JAMA. 1982;248:715-717. 95. Grangier C, Garcia J, Howarth NR, et al. Role of MRI in the diagnosis of insufficiency fractures of the sacrum and acetabular roof. Skeletal Radiol. 1997;26:517-524. 96. Stabler A, Beck R, Bartl R, et al. Vacuum phenomena in insufficiency fractures of the sacrum. Skeletal Radiol. 1995;24:31-35.

97. Cannada LK, Scherping SC, Yoo JU, et al. Pseudoarthrosis of the cervical spine: a comparison of radiographic diagnostic measures. Spine. 2003;28:46-51. 98. Hadjipavlou AG, Cesani-Vazquez F, Villaneuva-Meyer J, et al. The effectiveness of gallium citrate Ga 67 radionuclide imaging in vertebral osteomyelitis revisited. Am J Orthop. 1998;27:179-183.

43

Thermal Applications

44

Lalaine Madlansacay Catapang, PT

Thermal or heat modalities have been popular treatments for soft tissue dysfunction and pain management for centuries. Hot baths, infrared lamps, water bottles, moist warm towels, warm compresses, ultrasound, and hot moist packs have been conventionally used for the treatment of muscle spasms and chronic pain. This chapter discusses the effects of heat on soft tissue and reviews the various types of heat modalities.

in the tissue temperature, and the size of the area being treated determine the extent of the physiologic response to heat.

Commonly Used Heat Modalities in Present Clinical Setting Hot Packs or Hydrocollator Packs

Physiologic Effects of Local Application of Heat Heat energy applied to a localized area of the body produces changes not only at the site of application, but also in surrounding tissues and in distant regions. The resultant changes counter the threat to thermal equilibrium and assist the local structures to avoid tissue damage. The local effects are caused by the elevated temperature response of cellular function by direct and reflex action. The rise in temperature is accompanied by an increase in blood flow. Dilatation of the capillaries on exposure to local heat leads to an elevation of hydrostatic pressure and an increase in capillary permeability. The increase in permeability leads to an increase in leukocytic and antibody infiltration in the area, which is an important factor in controlling inflammation and promoting early healing. However, an increase in hydrostatic pressure may cause edema of the desired region. This effect would contraindicate the use of heat in conditions where swelling or edema is to be avoided.1 Superficial heat remodels connective tissue by three mechanisms. First, heat creates several physiologic changes through subsequent vascular changes, causing vasodilation. This dilation gives an analgesic effect, which increases the patient’s pain threshold and results in greater tolerance of connective tissue stretching. Second, physiologic effect of heat is an alteration of the viscous flow properties of collagen, which results in the relief of joint stiffness. Third, there is an increase in the extensibility of collagen tissue, a major component of connective tissue, through changes in its viscoelastic properties following the application of heat.2 In general, the transfer of heat (whether the purpose is heating or cooling) often is classified into four general types of heat transfer: conduction (hot pack, paraffin bath), convection (fluidotherapy, hydrotherapy), conversion (radiant heat), and radiation. The most commonly used in clinical application is conduction, through the agency of water.1 The level of the tissue temperature (usually 40 to 45° C), duration of the tissue temperature increase, rate of increase

Hot packs or hydrocollator packs contain silica gel which is heated to a temperature of about 170° F. These packs are placed in a thermostatically controlled hot water tank. The silica gel absorbs a large quantity of water and has a high heat capacity. Hot packs are applied over 4 to 6 layers of towels between the pack and the patient. The recommended treatment time is for 20 to 30 minutes. The method of heating is through conduction. Heat transmitted to the patient increases during the first few minutes of treatment as the towels get heated. To prevent burning, adequate layer(s) of towel should be added during the duration of treatment and the patient should never lie on the packs because the patient’s body weight could squeeze hot water out of the pack into the towel and potentially cause a burn. It is highly recommended to check the patient every 5 minutes. Indications for the application of hot packs may include painful muscle spasms, abdominal muscle cramping, menstrual cramps, and superficial thrombophlebitis.3 Contraindications may include peripheral vascular diseases, skin eruptions at the site of application, desensitized skin, new skin, and obtunded sensorium of the patient.4 When applying the hot pack, have the patient remove clothing from the area to be treated. The patient is set in a comfortable position. The area to be treated can be supported or elevated when necessary. Apply one or several layers of towels to the area. Determine the wrapping procedure to be used. Apply the hot pack to the area to be treated. Cover it with a dry towel. Check the patient every 5 minutes (Figs. 44-1 to 44-3).

Ultrasound/Ultrasonic Therapy Ultrasound is the deepest heating modality used in physical therapy. The term ultrasonic refers to sound waves or vibrations that have a frequency above the audibility of the human ear. Therapeutic ultrasonography uses a frequency range of 0.8 to 1.0 MHz. Ultrasonographic energy is generated by the piezo-electric effect. Electrical energy is applied to a crystal causing the crystal 551

552  Physical Modalities for Pain Management

Figure 44-1  Hot moist pack treatment—neck and low back.

Figure 44-2  Hot moist pack treatment—neck and low back.

to vibrate at a high frequency and thereby to produce ultrasound waves. Ultrasound is delivered by continuous or pulsed highfrequency sound waves and provides a high heating intensity.3 The sound waves vibrate tissues deep inside the injured area. This creates heat that draws more blood into the tissues, which institutes the reparative process. Ultrasound is the optimal form of heat treatment for soft tissue injuries. It is used to treat joint and muscle sprains, bursitis, and tendonitis. Ultrasound can produce many effects other than just the potential heating effect. It has been shown to cause increases in tissue relaxation, local blood flow, and scar tissue breakdown. The effect of the increase in local blood flow can be used to help reduce local swelling and chronic inflammation, and, according to some studies, promote bone fracture healing. The intensity or power density of the ultrasound can be adjusted depending on the desired effect.5 Knight and associates6 studied the effects of superficial heat and deep heat including ultrasound on the extensibility of plantar flexors. The results indicated that among the modalities tested, the use of ultrasound for 7 minutes prior to stretching may be the most effective for increasing ankle dorsiflexion range of motion (ROM).

Figure 44-3  Hot moist pack treatment—left shoulder and right knee.

The equipment used for therapeutic application of ultrasonic energy consists of a generator of high-frequency current and an applicator, also referred to as an ultrasound head or transducer head. The generator produces electric oscillations of the desired frequency, which cause the head to vibrate and generate sound waves. The application needs a coupling medium between the transducer head and the skin such as ultrasonic gel or water. This allows the ultrasonic waves to pass through air and air-free contact must be established between the ultrasound head and the area being treated. The gel is applied to the area being treated and the applicator is gently moved over the skin with light pressure. Stroking motion is applied to larger areas such as the back or neck and circular motion is applied for smaller areas such as the shoulder, hip, or knee. Because the ankle/foot and wrist/hand have irregular surfaces, an underwater technique is recommended. When this technique is used, the ultrasound head is kept an inch away from the area being treated and slowly moved in a circular fashion. This would allow a uniform distribution of energy on the area being treated. Ultrasound can also be used in phonophoresis. This treatment involves the application of a topical antiinflammatory. The anti­ inflammatory medication can be mixed with the ultrasound gel and applied to the area using the ultrasound head. The ultrasonic sound waves force the medication to migrate into the tissues, thereby reducing inflammation. A typical ultrasound treatment will take from 3 to 5 minutes depending on the size of the area being treated. For underwater treatment, time is progressive, beginning at 5 minutes and increasing to a maximum of 8 to 10 minutes per treatment. The dosage depends on the intensity and time, and the product of these factors is usually expressed in watt-minutes. The intensity of sound energy available from the ultrasound head is usually expressed as watts per square centimeter. Therapeutic intensities of 0.5 to 2.0 watts per square centimeter have been determined to be useful.7 Ultrasound treatment series is considered to be 6 to 12 applications, applied daily according to some authorities. Others say, every other day. It is also important to remember that when using this modality in acute conditions, low intensity treatment is required. Chronic conditions will require a higher intensity. Ultrasound treatment, just like any other deep heating

Thermal Applications  553

44

Figure 44-4  Ultrasound treatment—low back, right paraspinal muscles.

Figure 44-5  Ultrasound treatment (underwater method)—right wrist and hand.

modality is used to (1) relieve pain and inflammation, (2) speed healing, (3) reduce muscle spasms, and (4) increase ROM. This treatment modality is commonly used for joint contractures, joint adhesions, calcific bursitis, hematoma resolution, and neuromas. Other conditions that may benefit from ultrasound treatment include fibrosis, phantom limb pain, myofascial pain, reflex vasodilatation, and ulcer débridement. However, the therapeutic benefit maybe limited in these later conditions. Warden and associates8 have shown that conventional therapeutic ultrasound as traditionally used by physical therapists may be used to ­accelerate fracture healing. Ultrasound treatment is contraindicated in the pregnant uterus, laminectomy sites, and ischemic areas. Application of ultrasound over surgically implanted hardware remains controversial and when performed in these areas it should be done with caution (Figs. 44-4 and 44-5).3

When performing the dipping method, the hand or foot is placed in the liquid paraffin bath and is withdrawn when a thin layer of warm, solid paraffin forms, becomes adherent, and covers the skin. This procedure is repeated 8 to 10 times until a thick paraffin glove is formed. By wrapping the body part with plastic wrap and towels for 20 to 30 minutes, the heat can be retained. A masking tape can be used to hold the towel in place. To remove the paraffin, slip finger under the upper edge and peel it off. Return the paraffin to the bath. The paraffin can be re-used. When performing the immersion method, initially perform the dipping method to form a protective covering of paraffin. Then immerse extremity for the prescribed time or until the paraffin is melted. Make sure the patient is rested in a relaxed position. Putting a padding on the edge of the tank will make the patient more comfortable during the treatment process (Figs. 44-6 to 44-9).

Paraffin Bath A paraffin bath is another form of conductive heating. Paraffin baths are particularly useful for contractures due to rheumatoid arthritis, burns, and progressive systemic sclerosis (scleroderma).3 Paraffin is usually applied to the hands, arms, and feet. Higher temperature (55° C) is tolerable without danger of burning the tissue when using paraffin as compared to water, (42° C to 45° C) because the specific heat is one-half that of water and solid paraffin forms a protective and insulating coat over the skin. For therapeutic purposes, the paraffin bath is maintained at the melting point of 51.7° C to 54.4° C in an insulated, thermostatically controlled container. Ayling and associates9 studied the efficacy of paraffin baths for rheumatoid arthritic hands. The results indicated that of the four randomized trials identified concerning the outcome of paraffin wax applications to rheumatoid arthritic hands, one yielded equivocal results, whereas three reported that after 3 to 4 weeks, paraffin wax applications were accompanied by significant improvements in rheumatoid arthritic hand function when followed by exercise. This modality also relieves pain and stiffness immediately after its application with no documented detrimental effects on the disease process, even though paraffin wax temporarily raises joint temperature. The method of application includes (1) dipping, (2) immersion, (3) brush application or paraffin pack or painting, (4) casting or wrapping, and (5) pouring. Dipping and immersion methods are more commonly used in the clinical setting.

Heat Treatment for Home Use Warm compresses or moist warm towels can be used at home. Preparation includes the following: (1) fold the hand towel lengthwise and then crosswise; (2) wet the towel and place it in a plastic bag; (3) put the bag in the microwave oven for 4 minutes; (4) wrap the bag in a dry towel and apply to affected area; (5) apply the warm compress for 10 minutes and repeat the same process twice to complete the 20-minute treatment (Fig. 44-10). Clinical Application of Heat Modalities Superficial and deep heat modalities are good preparatory treatments to most therapy procedures except for acute strains and sprains. Hot moist packs can be used before ultrasound treatment followed by stretching exercises or joint mobilization. After the soft tissues become pliable following superficial heat treatment, ultrasonic waves may then be used to provide optimal results. When soft tissues and muscles are flexible prior to exercise or joint mobilization, therapeutic goals may be obtained.

Conclusion Superficial and deep heat has been used by health care providers as a treatment of choice or as an adjunct modality prior to other regimens such as therapeutic exercise or joint mobilization. These treatments can provide pain relief and promote overall functional improvements.

554  Physical Modalities for Pain Management

Figure 44-6  Paraffin bath treatment, dipping method—right hand.

Figure 44-9  Paraffin bath treatment, immersion method—right hand.

Figure 44-7  Paraffin bath treatment, dipping method, wrapping the extremity with cellophane—right hand.

Figure 44-10  Warm compress treatment for home use.

REFERENCES

Figure 44-8  Paraffin bath treatment, dipping method, wrapping the extremity with towel—right hand.

1. Reyes T. Introduction to Physical Therapy and Patient Care, Hydrotherapy, Traction, and Massage. 2nd ed. Manila, Philippines: UST Press; 1985:121. 2. DiFrancesco B: Heat application in physiotherapy. Website. http://www. activebodyclinic.com/core_Physio_heat.html. Accessed August 23, 2009. 3. Klein M: Superficial heat and cold. Website: http://emedicine.medscape. com/article/324974-overview. Accessed August 23, 2009. 4. Reyes T. Introduction to Physical Therapy and Patient Care, Hyrotherapy, Traction, and Massage. 2nd ed. Manila, Philippines: UST Press; 1985:143. 5. Ultrasound in physical therapy. Website: http://www.automailer.com/ tws/ultrasound.html#ixzz0QeK81VD9. Accessed August 28, 2009. 6. Knight C, Rutledge C, Cox M, et al. Effect of superficial heat, deep heat, and active exercise warm-up on the extensibility of the plantar flexors. Phys Ther. 2001;81:1206-1214. 7. Shestack R. Handbook of Physical Therapy. 3rd ed. New York: Springer Publishing; 1977:47. 8. Warden SJ, Fuchs RK, Kessler CK, et al. Ultrasound produced by a conventional therapeutic ultrasound unit accelerates fracture repair. Phys Ther. 2006;86:1118-1127. 9. Ayling J, Marks R. Efficacy of paraffin wax baths for rheumatoid arthritic hands. Physiotherapy. 2000;86:190-201.

45

Cold (Cryo) Therapy Peter M. Chanliongco, PT

Superficial physical agents such as cold, heat, light, friction, and pressure have been used in therapy for thousands of years. Cryotherapy, or the use of cold, is restricted to superficial agents that are inexpensive, easy to use and requires little time to prepare, usually simple, but effective. Ice and cold water are the usual agents, but vaporizing liquids, refrigerated units, and chemical packs may also be used. The application of ice to an injury, in the acute phase can substantially decrease the extent of the damage. Even though treatments are restricted to superficial application; cold therapy may produce longer-lasting physiologic changes than are possible from heat treatments of similar intensities.1

Biophysics Chilling a limited portion of the body results in a number of local and distant physiologic changes. Although there is some controversy,2 most clinicians feel that there is an initial period of vasoconstriction due to the local reflexes and increased sympathetic constrictor tone.3,4 Vasoconstriction is thought to continue until subcutaneous temperatures fall to about 15° C/59° F. Below 15° C/59° F, vessels dilate, probably as a result of contractile mechanism paralysis or blockage of constrictor signals. An oscillating “hunting” pattern of constriction and reactive hyperemia may occur, at least in the digits, as was described by Lewis.2,3 At 0° C/32° F, skin blood flow may be greater than normal. If the cooling agent is ice, skin temperature will initially decrease rapidly and then will more slowly approach as equilibrium temperature of about 12 to 13° C/54 to 55° F in 10 minutes. Subcutaneous temperatures decline more smoothly and in 10 minutes will fall to 3 to 5° C/37 to 41° F. Deep muscle temperatures decrease the least, and in 10 minutes may lessen by a degree or less.5 Chilling for longer periods result in more pronounced effects and intramuscular forearm temperature decreases of 6 to 16° C/43 to 61° F are reported following periods of 20 minutes to about 3 hours of vigorous cooling.6,7,7a Vasoconstriction reduces blood flow and the return of cooled tissue to normal temperatures is slower than in heated and hyperemic tissue. The amount of energy that tissue will gain or lose during treatment depends on the nature of the tissue itself, the treatment modality involved, and the duration of exposure. In addition, the body places physiologic limits on the amount of cold it will tolerate. For example, exposure of skin to temperatures below 13° C/55° F are uncomfortable, and if the body is cooled below 28° C/82.4° F, death may occur.3

Effects of Cold Therapy Pain Relief The reason behind the application of ice resulting in pain relief is not clear. There are many theories and it is possible that a number of proposed mechanisms in combination can cause pain relief.7b,7c Some of the possible mechanisms include the following: Cold decreases nerve transmission in the pain fibers Cold reduces the activity of nerve endings1 ll Cold causes a release of endorphins ll Cold raises the pain threshold ll Cold sensations override the pain sensation ll ll

Reduction of Bleeding and Swelling By cooling the surface of the skin and the underlying tissues, ice causes the narrowing of the blood vessels, a process known as vasoconstriction. The vasoconstriction leads to a decrease in the amount of blood being delivered to the area and, subsequently, lessens the amount of swelling. After a number of minutes, the blood vessels reopen (dilate) allowing blood to return to the area. This phase is followed by another period of vasoconstriction—this process of vasoconstriction followed by dilation is known as the hunting response.

Reduction of Muscle Spasm Muscle spasm is often a response to pain. The muscles surrounding an injury contract to protect the underlying tissue (muscle guarding) and prevent further damage.7e,7f,7g Ice, being useful for pain relief, is therefore advantageous in reducing muscle spasm. In addition, muscle overuse or imbalances can be improved through the use of cold therapy. This mechanism is not fully understood, but is believed to be due to ice slowing conduction velocity of sensory and motor nerves, as well as the activity of muscle spindle cells (responsible for muscle tone), resulting in a decrease in motor activity.

Slowing of the Metabolic Rate By reducing the metabolic rate, ice reduces the oxygen requirements of the cells. Thus, when blood flow has been limited by vasoconstriction, the risk of cell death due to oxygen demands (secondary cell necrosis) will be lessened. 555

556  Physical Modalities for Pain Management

General Indications for Cold Modalities Acute musculoskeletal trauma (e.g., edema, hemorrhage, analgesia) ll Pain ll Muscle spasm ll Spasticity ll Adjunct in muscle reeducation ll Reduction of local and systemic metabolic activity ll

General Precautions and Contraindications for Cold Modalities Ischemia Cold intolerance ll Raynaud phenomenon and disease ll Severe cold pressor responses ll Cold allergy ll Insensitivity ll

of an ice pack containing at least 0.6 kg of ice leads to a greater magnitude of cooling compared with application of a 0.3 kg ice pack, regardless of the size of the contact area.14

How to Apply Cold Therapy There are numerous methods that can be used to apply different forms of cold therapy. Each type has its benefits and limitations. The decision to use one form over another depends on the body part to be cooled and the type of injury. This section will give you background on each technique to allow you to make the best choice to relieve pain and restore function. An important precaution is to discontinue cold therapy when the skin feels numb.

ll

Research Studies Taber,8 and others have evaluated local vascular response during cryotherapy. Their study was performed to determine whether application of a cold pack reduced blood volume in a nontraumatized ankle. Changes in local blood volume at the ankle were measured over a 20-minute period for the following three conditions: rest, room-temperature gel pack application, and cold gel pack application. A significant reduction in local blood volume was found for the cold gel pack condition in comparison with the resting condition. Maximum decrease in blood volume occurred at 13.5 minutes after cold gel pack application. Reactive vasodilation was not observed. The results lend support to the clinical use of a cold gel pack when a reduction in local circulation is desired, such as in the management of acute-phase soft tissue trauma.8 Belitsky,9 and others compared the ability of wet ice (WI), dry ice (DI), and cryogen packs (CGPs) to reduce and maintain the reduction of skin temperature directly under the cooling agent and to determine whether the cooling effect on skin extended beyond the surface area in contact with the cooling agent. Each of the three cold modalities was applied randomly to the skin overlying the right triceps surae muscle. The only significant differences in cooling were between WI and DI and between WI and CGP. Fifteen minutes after removal of the cold modalities, no significant differences were found in mean skin temperature between WI, DI, and CGP. No cooling was demonstrated 1 cm proximal or distal to any of the cooling agents after 15 minutes of cold application. Akgun and colleagues10 concluded that with increased cold gel pack application time, the duration of cooling effect increased while the deep tissue temperature decreased. The length of application time and the duration of cooling effect were not linearly related. This ratio decreased progressively after 20 minutes. The ice pack and mixture of water and alcohol were found to be significantly more efficient in reducing skin surface temperature than the gel pack and frozen peas.11 Cold whirlpool was found to be superior to crushed-ice packs in maintaining prolonged significant temperature reduction after treatment.12 Wetted ice was found to be superior to cubed or crushed ice at reducing surface temperatures, whereas both cubed ice and wetted ice were superior to crushed ice at reducing intramuscular temperatures.13 Application

Ice Packs/Bags An ice pack is any type of container that holds crushed or chipped ice. This technique uses simple bags such as a plastic bag, towel, especially designed ice bag, or frozen vegetables (bag). Technique— Dry the area first. Apply a dry terry cloth towel over the area to prevent direct contact of the ice to the skin. Apply your choice of cold to the area for no more than 20 minutes. The skin will pass through four stages of sensation in 10 to 15 minutes. These sensations in order are (1) cold, (2) burning, (3) aching, (4) numbness.

Ice Baths An ice bath can easily be made by half-filling a large container/tub with cold water and ice. The size of the container and depth of the water required depends on the body part to be treated. This is the best method of cooling awkward, bony areas, such as the foot, ankle, hand, and elbow. Immediately following injury, submerging the injured body part may not be as beneficial as using a cold pack and compression wrap because there is no compression (RICE principle—rest, ice, compression, and elevation). Wrapping the ankle prior to submersion will also prevent maximal cooling by insulating the body part (see Fig. 45-1).

Ice Massage Ice massage is another cold (cryo) therapy technique. Place clean tap water into a foam cup, or specially designed cup and place in your freezer until it is completely frozen. Peel back a small amount

Figure 45-1  Ice bath.

Cold (Cryo) Therapy  557

of the top of the cup and massage this onto the area of pain using constant circular motion. Do not hold the ice in one area for more than 3 minutes because this may cause frostbite. Ice massage therapy can be repeated two to three times a day (see Fig. 45-2).

because they are reuseable and not as messy as ice packs. However, when taken out of the freezer, they immediately begin to thaw and so are not suitable for use on the field of play. They must also be applied to the skin through a towel or cloth to prevent frostbite (see Fig. 45-3).

Gel Packs These commercially available packs contain a gelatinous substance, which is kept frozen in a freezer until required. Better examples contain some form of anti-freeze which prevents the gel from freezing into a rigid position, allowing the pack to be molded to the shape of the body part. These are good for use in a clinic setting

Chemical Cold Packs These are single-use cold packs where compressing and rupturing a central pouch, contained within the pack, releases a second chemical which causes a reaction that lowers the temperature of the pack. These packs do not lower in temperature enough to significantly reduce tissue temperature. They are, however, convenient for emergency use.

Vapocoolant Sprays These sprays evaporate quickly when they come into contact with the skin. This removes heat from the skin at the same time. They result in only a very superficial cooling effect. This method is commonly used by physicians, therapists, or athletic trainers in the “spray and stretch technique” —involving the application of prescription vapocoolant spray at a tender site to help deaden a painful sensation while contracted muscle is being stretched.

Cryocuff

Figure 45-2  Ice massage.

The Cryocuff is a machine that consists of a gallon tank of ice water and a nylon sleeve, into which you place the injured part. The ice water flows through the cuff to cool the body part. The tank must be raised to allow more water to flow into the cuff and increase the pressure. In this way, compression is also applied to the injury.

A

B

C

D Figure 45-3  Gel packs.

45

558  Physical Modalities for Pain Management

Figure 45-4  Cryocuff.

To cool the water sitting in the cuff, the tank is lowered to allow it to flow back into the tank where it mixes again with the ice water. The tank can then be raised again to fill the cuff. The Cryocuff allows a good degree of cooling and compression, is relatively portable, and is reuseable. Different shapes and sizes of cuff can be used to allow for all body parts (see Fig. 45-4). As with all pain relief treatments, ice or a cold pack should be applied for no more than 20 minutes at a time and can be applied several times a day (e.g., up to eight or ten times in a 24-hour period).

Conclusion Cryotherapy decreases the amount of bleeding by vasoconstriction into the injury site, thereby reducing swelling, pain, and the risk of cell death. Cryotherapy also reduces the rate of metabolic activity, lessens muscle tone, and inhibits spasticity and clonus.7,15,16 This form of treatment has also been shown to increase gastrointestinal motility,17 slow nerve conduction, and produce analgesia. Any type of cold application should be stopped when the skin feels numb. REFERENCES   1. Basford JR. Physical agents and biofeedback. In DeLisa JA, Currie DM, Gans BM, et al. Rehabilitation Medicine: Principles and Practice. Philadelphia: JB Lippincott, 1988:257-271.   2. Knight KI. Circulatory effects of therapeutic cold applications. In: ­Cryotherapy: Theory, Technique and Physiology. Chattanooga, Tenn: Chattanooga Corp; 1985:83-100.   3. Franchimont P, Juchmes I, Lecomite J. Hydrotherapy—Mechanism and Indications. Pharmacol Ther. 1983;20:79-93.   4. Guyton AC. Muscle blood flow during exercise: Cerebral, splanchnic, and skin blood flows. In: Guyton AC, ed. Textbook of Medical Physiology. Philadelphia: WB Saunders; 1986:336-346.

  5. Lehmann JF, deLateur BJ. Diathermy and superficial heat and cold therapy. In: Kottke FJ, Stillwell GK, Lehmann JF, eds. Krusen’s Handbook of Physical Medicine and Rehabilitation. Philadelphia: WB Saunders; 1982:275-350.   6. Alcorn R, Bowser B, Henley EJ, Holloway V. Fluidotherapy and exercise in the management of sickle cell anemia. A clinical report. Phys Ther. 1984;64:1520-1522.   7. Hartviksen K. Ice therapy in spasticity. Acta Neurol Scand. 1962;38: 79-84. 7a. Brown WC, Hahn DB. Frostbite of the feet after cryotherapy: A report of two cases. J Foot Ankle Surg. 2009;48(5):557-580. 7b. Ebersold MJ, Laws ER, Stonnington HH, Stillwell GK. Transcutaneous electrical stimulation for treatment of chronic pain: A preliminary report. Surg Neurol. 1975;4:96-99. 7c. Greenstein G. Therapeutic efficacy of cold therapy after intraoral surgical procedures: A literature review. J Periodontal. 2007;78(5):790-800. 7d. Abramson DI, Chu LS, Tuck Jr S, et al. Effect of tissue temperatures and blood flow on motor nerve conduction velocity. JAMA. 1966;198:1082-1088. 7e. Harris ED Jr, McCroskery PA. The influence of temperature and fibril stability on degradation of cartilage collagen by rheumatoid synovial collagenase. N Engl J Med. 1974;290:1-6. 7f. Wright V, Johns RJ. Quantitative and qualitative analysis of joint stiffness in normal subjects and in patients with connective tissue diseases. Ann Rheum Dis. 1961;20:36-46. 7g. Lehmann JF, Masock AJ, Warren CG, Koblanski JN. Effect of therapeutic treatments on tendon extensibility. Arch Phys Med Rehabil. 1970;51:481-487.  8. Taber C, Contryman K, Fahrenbruch J, et al. Measurement of reactive vasodilation during cold gel pack application to nontraumatized ankles. Phys Ther. 1992;72:294-299.   9. Belitsky RB, Odam SJ, Hubley-Kozey C. Evaluation of the effectiveness of wet ice, dry ice, and cryogen packs in reducing skin temperature. Phys Ther. 1987;67(7):1080-1084. 10. Akgun K, Korpinar MA, Kalkan MT, et al. Temperature changes in superficial and deep tissue layers with respect to time of cold gel pack application in dogs. Yonsei Med J. 2004;45(4):711-718. 11. Kanlayanaphotporn R, Janwantanakul P. Comparison of skin surface temperature during the application of various cryotherapy modalities. Arch Phys Med Rehabil. 2005;86(7):1411-1415. 12. Myer JW, Measom G, Fellingham GW. Temperature changes in the human leg during and after two methods of cryotherapy. J Athl Train. 1998;33(1):25-29. 13. Dykstra JH, Hill HM, Miller MG, et al. Comparisons of cubed ice, crushed ice, and wetted ice on intramuscular and surface temperature changes. J Athl Train. 2009;44(2):136-141. 14. Janwantanakul P. The effect of quantity of ice and size of contact area on ice pack/skin interface temperature. Physiotherapy. 2009;95(2): 120-125. 15. Knutsson E, Mattson E. Effects of local cooling on monosynaptic reflexes in man. Scand J Rehabil Med. 1969;1:126-132. 16. Miglietta O. Action of cold on spasticity. Am J Phys Med. 1973;52: 198-205. 17. Bisgard JD, Nye D. The influence of hot and cold application upon gastric and intestinal motor activity. Surg Gynecol Obstet. 1940;71:172-180.

Electrical Stimulation

46

Albert C. Recio, MD, RPT, PTRP, and Anna C. Schneider, BS Historical Perspective Long before the development of modern electricity, “natural electricity” was used for its therapeutic properties of inducing analgesia. In the earliest written description of an electric fish, Aristotle remarked, “The torpedo is known to cause a numbness even in human beings.”1 Perhaps the earliest record of local electrical analgesia was when Scribonius Largusm wrote in circa CE 46 that he advocated piscine “electrotherapy” for the relief of pain.1 Centuries later, in the mid 1740s, the application of an electrical apparatus was first used in medicine by Kratzenstein.1 In 1858, Francis received a patent for an electrical device that he claimed relieved dental pain; he boasted that he had performed 164 successful tooth extractions and that most had resulted in no pain.1 Despite its long history, the use of electrical signals for clinical application has not been a widely accepted theory throughout the history of modern medicine. But since the 1960s, when Melzak and Wall pioneered the gate theory of pain, advancements in the field of electrical stimulation for pain management have come rapidly. Clinical and scientific analysis has led to a systematic collection of data that has defined the beneficial use of electrical stimulation in the clinical setting.

Electrical Stimulation in Modern Medicine As a physical modality, electrical stimulation has been prescribed to strengthen muscles, promote healing, decrease urinary incontinence, and increase circulation, as well as for pain management.2 Electrical stimulation is a nonpharmacologic and, in most cases, a noninvasive pain-management method that has been promoted for its analgesic properties. It has demonstrated efficacy for a variety of pain conditions including chronic low back pain,3-4 dysmenorrhea,5 hemiplegic shoulder pain,6 and arthritic pain.40 In all three types of electrical stimulation that will be explored in this chapter, an electrical stimulation device is turned on and electrical current is sent through electrodes that are applied to the body causing a tingling sensation and/or muscle contractions in the underlying skin and muscle. This electrical signal disrupts the regular pain signals that are being sent from the affected area to its surrounding nerves. By interrupting this signal pathway, the recipient perceives less pain (see Fig. 46-2). The most well known method of electrical stimulation, transcutaneous electrical stimulation (TENS) is a generic term used to describe a type of electrotherapy that applies low-voltage electrical

pulses to the nervous system using surface electrodes placed on the skin around the affected area. Because of the variability of frequency, amplitude, voltage, pulse width, and/or pulse rate, TENS has stemmed into several different techniques. By using one or more of these variables, patients and practitioners can be allowed to design four different TENS protocols including conventional TENS, acupuncture mode TENS, burst TENS, and modulation TENS. Neuromuscular Electrical Stimulation (NMES), sometimes known as Electrical Muscle Stimulation (EMS), is often referred to as functional electrical stimulation (FES) when it is used to activate paralyzed muscles in a precise sequence and magnitude so as to directly accomplish functional tasks.6,8 Beyond its neurorehabilitation potential, NMES has shown efficacy in pain management. NMES uses high-intensity electrical stimulation to elicit intermittent contraction and relaxation of proximal muscle fibers and is widely prescribed following surgery and trauma. Developed in the early 1950s, interferential current (IFC) therapy produces two alternating currents of slightly differing medium frequency using wave interference to create a resultant amplitude of therapeutic stimulation.9 Interferential current therapy is mainly used to relieve pain that is felt in deep tissues. Depending on the configuration of the electrodes applied to the skin, the effects can be localized or adjusted to be more general. Unlike other methods of low-frequency electrical stimulation, IFC encounters low electrical resistance and therefore can penetrate deeply without causing unnecessary discomfort. Electrotherapeutic modalities are typically administered by physical therapists and physicians in a variety of clinical settings, including private practice, rehabilitation centers, and hospitals. Some units may be used in the home care setting following education by a clinician and those can be obtained directly by the patient or via the health care professional. Electrotherapeutic devices are regulated by the Food and Drug Administration (FDA) but generally require less evidentiary support than a new drug or surgical device for marketing approval. This chapter will discuss in detail the uses, contraindications, mechanisms, techniques, and safety precautions involved with TENS, NMES, and IFC in pain management. We will also explore its evidence of efficacy and clinical acceptance.

Transcutaneous Electrical Nerve Stimulation TENS is a method of pain relief in which a device transmits lowvoltage electrical impulses through electrodes on the skin to an area of the body that is in pain. 559

560  Physical Modalities for Pain Management

Proposed Mechanisms of Pain Control Research indicates that TENS can be a noninvasive, safe method for managing and reducing both acute and chronic pain. Although a uniform mechanism has not been established, there are a number of theories to explain the modulation of pain associated with TENS. Two main theories on pain transmission are the gate theory and the endorphin theory.10 The gate theory pioneered by Melzack and Wall has been attributed to motivating the development of electrotherapeutic equipment, and the endorphin theory has led to a decrease on the reliance of pain medication for treatment of postoperative pain. An additional theory includes the acupuncture theory, which hypothesizes that management of pain is related to energy lines and its associated acupuncture points.

Gate Theory The gate theory asserts that stimulation of large, highly myelinated (afferent A-beta fibers) block the transmission of pain signals by relatively small, nociceptive fibers with little or no myelination (A-delta and C fibers) at the level of the spinal cord. Small, unmyelinated C fibers are responsible for chronic, throbbing pain, whereas the thicker A-delta fibers with slight myelination make them more conducive to transmitting faster more intense pain information. It is postulated that electrical stimulation decreases the perception of pain by increasing the activation of A-beta fibers and therefore flooding the pain signal pathway and ‘closing the gate’ of transmission in the spinal cord.11,12 These target cells are located in the substantia gelatinosa (Rexed’s laminae I, II, and IV) of the dorsal horn (Fig. 46-1).11,13

Thalamus 5 Analgesia is achieved

4 The C (small, nociceptive) fiber signals are stopped at the gate and the pain signals are not transmitted to the thalamus

3 The gate swings closed

2 These signals flood the pathway and stimulate the substantia galatinosa in the dorsal horn of the spinal cord

Pain

1 Myelinated A-beta fibers are activated

+ Electrical stimulation Figure 46-1  Simplistic view of the gate control theory. Pain signals are blocked at the spinal cord level before they can be transmitted by the thalamus and perceived by the individual.

Electrical Stimulation  561

Endorphin Theory Also known as the opiate-mediated theory, the endorphin theory is based on the discovery of the presence of natural opiates in the body (Fig. 46-2).14,15 Acting as the body’s own natural pain relievers, they are produced in the spinal cord and pituitary gland as enkephalins and beta-endorphins, respectively. These endogenous opiates are effective at decreasing the perception of pain and, in turn, mimicking the action of narcotic drugs. Basic science studies show that high and low-frequency TENS produce their effects by activation of opioid receptors in the central nervous system. High-frequency TENS and low-frequency TENS activate delta-opioid and mu-opioid receptors, respectively, both in the spinal cord and supraspinally (in the medulla). Studies suggest that TENS also stimulates the body’s production of endogenous opiates that interact with specific receptor cites in the central and peripheral nervous systems, thereby blocking the perception of pain. Cheng and Pomerantz demonstrated that pain relief produced at 4 Hz of stimulation (low frequency) was blocked by the opiate antagonist, naloxone, whereas pain relief induced at 200 Hz was not blocked by naloxone. When administered with a strong, subnoxious intensity at an adequate frequency, TENS has been demonstrated to decrease reliance on pain medication for postoperative pain.16-22 Acupuncture Theory A lesser-known theory that has been presented as a possible explanation for the ability of TENS to be effective in pain management is the acupuncture theory. Some believe that the use of TENS opens and stimulates common acupuncture points along the same meridians or energy lines used in traditional acupuncture. Acupuncture points can lie on, be adjacent to, or be distant from the site of pain. When applied to these points, TENS is believed to modify the flow of energy or chi resulting in a decrease in pain.23,24

PLACEBO (psychosocial context)

Rostral anterior cingulate cortex and orbitofrontal cortex

Nonopioid mediators CCK +

Endogenous opioids

– PAIN

–

Periaqueductal Pituitary gland gray 5-HT dependent GH and ACTH secretion Pons medulla

Respiratory – centers

Cortisol Adrenal glands

? + – β-adrenergic sympathetic system Heart

Figure 46-2  The placebo effect: pain inhibitory network owing to placebo. A descending pain-blocking network that involves the rostral anterior cingulate cortex, the orbitofrontal cortex, the periaqueductal gray, and the pons/medulla are activated. It is believed that endogenous opioids also act along this same pathway.

Some theorists propose that hyperirritable spots in the skeletal muscle that are associated with palpable nodules in taut bands of muscle fibers, known as trigger points, can be stimulated by TENS to successfully decrease pain. It is believed that trigger points cause tissue ischemia and that the application of TENS causes vasodilation to occur, which modifies the ischemic area, thereby decreasing pain.25-28

Practical Application Electrode Placement for TENS Electrodes may be placed over peripheral nerves, nerve roots, and acupuncture points, as well as proximal to, distal to, over, and (more controversially) contralateral to the areas of pain. The usual practice is to apply the electrodes to where the pain is felt. It can be applied with a dermatome, sclerotome, or myotome where the pain is felt, or even over a trigger or acupuncture point. Clinical Use and Application There are two basic types of units available. Marketed to consumers, the simplified version offers LCD screens and digital control with a range of preset programmers. The more complex units are the professional versions that do not have presets but allow frequency and pulse width settings to be varied to suit individual patient needs. There are four main types of stimulation (Table 46-1) namely: conventional mode TENS, acupuncture mode TENS, burst or pulse mode TENS, and modulation mode TENS. Conventional Mode TENS This mode has high-frequency (40 to 150 Hz) and low intensity (10 to 30 mA) stimulation, with amplitude being adjusted to induce minimal sensory discomfort. Studies have shown it is the most effective type of stimulation. This mode is most useful for neuropathic pain. Patients customarily apply the electrodes and have them in place all day, turning it on for approximately 30-minute intervals throughout the day. This mode activates A-beta and A-alpha nerves that cause interneurons from the substantia gelatinosa to inhibit the transmission of pain by T cells in lamina V neurons of the spinal cord (Table 46-2). Acupuncture Mode TENS Characterized as low-frequency (1-10 Hz) and high-intensity (close to the tolerance limit of the patient) stimulation, Acupuncture mode TENS is useful for musculoskeletal pain. It is thought that this mode stimulates C-fibers causing counterirritation. This method is often considered for patients who do not respond to conventional TENS. Acupuncture mode stimulates the hypothalamus which, in turn, causes the release of endogenous opiates, specifically beta-endorphin, evidenced by the fact that the TENS effect can be reversed by naloxone (see Table 46-2). Burst or Pulse Mode TENS In this mode, the unit delivers high-frequency stimulation bursts interrupted by low-frequency intervals. The recurrent burst discharge at 1 to 2 or 2 to 3 Hz and the frequency of the impulses with each burst is at about 100 Hz. There is a delayed onset of analgesia with this type of TENS, and no particular advantage has been established for pulse method over the conventional method. Like the acupuncture mode, burst mode causes the body to release endogenous opiates (see Table 46-2).

46

562  Physical Modalities for Pain Management

Table 46-1  Comparison of Various TENS Modes Conventional

Acupuncture

Burst

Modulation

Nature

High frequency Low intensity

Low frequency High intensity

Train or series pulses 1-5 times/sec

Pulse duration, frequency, and intensity all constantly varied

Major Purpose

Comfortable tingling   sensation Limited carry-over effect

Induce the production of endogenous opiates Higher carry-over effect

Stimulate the pain gate   and opioid mechanism

Decrease nerve or perceptual accommodation effects to stimuli

Pulse Width Duration (μsec)

40-125

200-500

200-500

Varies

Pulse Rates (pps) Frequency

50-100

1-5

1-5 burst/sec Each burst has seven pulses set between 70 and 100 pps

Varies

Amplitude

Submotor amplitude with a resultant numbness or tingling

Enough to cause local muscle contraction

Enough to cause muscle contraction

Varies

Advantages

Produces analgesia quickly Comfortable No motor response Can be used for a full day

Longer carry-over Slight adaptation

Same carry-over as low frequency More comfortable than   low frequency

Decrease nerve adaptation Comfortable, fast No motor response Can be used for a full day

Disadvantages

Short carry-over Adaptation can occur

May be uncomfortable due to forced motor response Not for acute conditions May limit patient’s functionality while on electrical stimulation Stimulation limited to 1 hr Analgesia delayed for 2-30 min

Same as low frequency (motor response more comfortable)

Short carry-over Constant change can be annoying

Indications

Acute or chronic pain Acute due to superficial cause

Acute or chronic Longstanding, deep pain

Acute or chronic

Acute or chronic

Prescription/Frequency of Treatment

Once or twice daily (30-60 min per session) May be 24 hr for postoperative pain Short pulses at 0.05 msec at 40-150 Hz Gradually increase intensity until paresthesia No pain or muscle contraction

Once a day for 60 min 0.2 msec at 2 Hz Intensity close to patient threshold 20-30 min every day

Frequency is adaptable to maintain pain-free state as long as possible Burst lasts 70 msec and pulses range from 50-100 Hz

Same as conventional

Modulated Mode TENS Pulse duration, frequency, and intensity all are constantly varied in an attempt to avoid neurohabituation in this particular mode. Because of the constantly changing stimuli, perceptual adaptation (which can occur under the use of constant unchanging stimuli) is decreased. Modulation mode works by the same mechanism as the conventional mode, which is closely related to the gate theory (see Table 46-2).

Neuromuscular Electrical Stimulation Neuromuscular electrical stimulation uses low-frequency, lowamplitude electrical current to targeted muscle groups to activate motoneurons, resulting in involuntary muscle contraction. NMES

Table 46-2  Precautions for Use of a TENS Unit External use only Keep from children Skin irritation at electrode placement sites Avoid water content

uses high-intensity electrical stimulation to elicit intermittent contraction and relaxation of proximal muscle fibers.29 Clinical NMES systems stimulate either the nerve directly or the motor point of the nerve proximal to the neuromuscular junction. Most clinical NMES systems fall into two broad categories: surface (transcutaneous) and implanted (usually percutaneous) systems.6 NMES

Electrical Stimulation  563

systems are either voltage or current regulated. Despite variable motor response, voltage-regulated stimulation is more common with transcutaneous NMES systems because, as resistance increases (due to electrode-to-skin interface changes), the current decreases.29

Proposed Mechanisms of Pain Control Like TENS, NMES is associated with gate theory and endorphin theory as possible explanations for the mechanism of analgesia owing to stimulation. It is believed that because NMES provokes muscle contractions in the applied area, it acts as a counterirritant stimulus, reduces muscle spasms, and increases muscle strength and endurance.3 It is believed that NMES reduces pain through muscle toning, and prevents disuse atrophy and muscle degeneration that is frequently associated with chronic myofascial pain.29

Practical Application Electrode Placement for NMES The most commonly used NMES electrode is the transcutaneous electrode that is applied to the skin and stimulates directly over the peripheral nerve or motor point of the targeted muscle groups. Two electrodes, which are placed in a monopolar or bipolar configuration, are required to produce an electrical current flow.6 However, trans-NMES for the treatment of some pain conditions, such as hemiplegic shoulder pain, has not been widely accepted due to stimulation-induced pain (because it can activate the subcutaneous pain fibers), poor muscle selectivity, and difficulty in daily application of electrodes.30 When used to treat shoulder subluxation, Yu and colleagues found that percutaneous-NMES was less painful than transcutaneous-NMES31 because tissues with C-fiber nociceptors that respond to strong mechanical, thermal, and chemical stimuli lie between the electrode and the muscle motor point making stimulation of these nociceptors difficult to avoid. Therefore, some practitioners and patients choose the minimally invasive percutaneous intramuscular electrodes that can reduce the risk of tissue injury. But with percutaneous-NMES systems, there is a risk of displacement or breakage associated with the anchoring of the external lead and electrode-related infection and granuloma formation secondary to retained electrode fragments. All percutaneous electrodes are anchored in place for the duration of the treatment. The electrodes then connect to lead wires that exit the skin and connect to the stimulator; this system eliminates skin resistance, cutaneous pain issues, allows greater muscle selectivity, and allows use of lower stimulation currents.6 Clinical Use and Application The external stimulation machine is connected to external leads that attach to the electrodes (either transcutaneous or percutaneous) using low-frequency, variable pulse delivery, and variable low amplitude. The electrodes are placed on or near a chosen target muscle group. Once a desired time (in seconds) for both the oncycle and off-cycle is chosen, the practitioner or patient will adjust the amplitude from 0 to 100mA until muscle contraction of the target group is achieved. Sometimes confused with acupuncturelike TENS, NMES uses a shorter pulse width, higher frequency, and has a cycle-on and cycle-off setting rather than continuous stimulation.

Interferential Current Stimulation Interferential stimulation is primarily effective in allowing deeper tissue penetration extending over a larger tissue volume than TENS is capable of stimulating.39 This technique differs from TENS in that it uses two alternating currents of slightly different medium frequency. When two or more sinusoidal currents are in phase, they alternate at the same frequency, rising and falling at the same time. Waves become out of phase when the falling of one wave corresponds to the rise of the other. Waves in phase interfere constructively to produce a resultant wave with the amplitude greater than the originals. Waves out of phase interfere destructively to cancel one another out. IFC applies these principals by using waves of a slightly different frequency. As one wave peak catches up to the other, constructive interference occurs, causing an increase in resultant amplitude; conversely, this resultant amplitude decreases as the waves drift out of phase and interfere in a destructive manner (Fig. 46-3). The rate or ”beat frequency” at which the resultant amplitude rises and falls depends on the difference between the two frequencies being used. This resultant amplitude’s frequency or beat frequency is actually the therapeutic stimulation.9

Proposed Mechanisms of Pain Control All of the electrical stimulation methods described in this chapter are believed to be effective owing to the gate and endorphin theories of pain. But because of the different current flowing between each pair of electrodes in IFC, it is speculated to have an even more complex mechanism. Although the current flowing between each pair of electrodes is insufficient to stimulate nerve and muscle directly, when amplitude is modulated by interference, IFC creates a deeper signal.

l 0 –l

4050 Hz current 1

l2 0 –l 2

4000 Hz current 2

(l + l 2 )

0

(4050–4000 Hz) = 50 Hz resultant current

–(l 1 + l 2 ) Figure 46-3  Modulation of amplitude caused by alternating current that creates interference.

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Wedensky Inhibition Repetitive stimulation at any frequency of at least 4000 Hz up to its maximum will cause action potentials to flow in the axon at the same rate. As the rate of stimulation increases above this value, successive stimuli fall within the relative and eventually the absolute refractory period of the preceding action potential. Therefore, a larger than normal flow of current is needed to stimulate a refractory neuronal membrane and thus the sensitivity of the nerve decreases. Prolonged stimulation at a supramaximal frequency will cause Wednesky inhibition of type C nociceptive fibers, eventually causing the axon to cease conducting. Accommodation of the neuron is responsible for this effect, caused by an increased threshold for pain and synaptic fatigue.9

45° Circuit 2 unmodulated

Practical Application Electrode Placement Most units use four electrodes to be placed at four corners around the area to be stimulated, with pairs using the same frequency at opposite corners. The stimulated area will then be a four-leaf clover-shaped area with the clover leaves at a 45-degree angle to the resultant intersection of the opposing frequencies (Fig. 46-4). Clinical Use and Application Like TENS and NMES, IFC uses two pairs of electrodes but one pair of the electrodes has a fixed frequency of 4000 Hz, whereas the other has a variable frequency between 4000 Hz and 4250 Hz. The variable electrode is then amplified to a therapeutically useful intensity. Some units operate at a base frequency of 2 kHz, which some practitioners believe can stimulate muscles more effectively.9

Safety Precautions for Electrical Stimulation There are many safety concerns when considering the application of electricity directly to the human body. TENS, NMES, and IFC are contraindicated for use over the anterior cervical region, carotid sinuses, heart, transthoracic area, insensate skin, and the abdomen of a pregnant woman. Electrodes should never be placed on or near the eyes, in the mouth, transcerebrally, on the front of the neck. Electrical stimulation should not be used by people with an artificial demand-type cardiac pacemaker owing to risk of interference and failure of the device (Table 46-3).9 It is not to be used on anyone with an implanted defibrillator, or any other implanted electrical device.32 Stimulation should not be done during electrocardiogram testing or while operating diathermy devices. Electronic stimulation should not be used over swollen, infected, or inflamed areas or skin eruptions (e.g., phlebitis, thrombophlebitis, varicose veins). Patients may report discomfort or skin irritation if the intensity is too high; skin irritation can be resolved if electrode positions are shifted or if a different conducting gel is used (see Table 46-2).

Evidence of Efficacy TENS A 2008 systematic review conducted by Poitras and Brosseau in the relief of nonspecific or rheumatic chronic lower back pain (CLBP) identified six randomized controlled trials on the use of TENS. Number and length of treatment sessions varied among studies,

Resultant current 100% amplitude modulation

Circuit 1 unmodulated

Figure 46-4  Quadripolar electrode placement and resultant amplitude stimulation owing to the pattern of interference current produced.

Table 46-3  Common Indications and Contraindications for Use of TENS Common Indications

Common Contraindications

Diabetic neuropathic pain

Stimulation over the carotid sinuses

Posttraumatic pain

Cardiac pacemakers (controversial)

Postsurgical pain

Pregnancy (although risk from distal treatment appears to be negligible)

Peripheral nerve injury

Inability to report effects or discomfort

Chronic musculoskeletal pain

Atrophic skin

Phantom limb pain

Allergies to electrodes or gels

Sympathetically mediated pain (reflex sympathetic dystrophy, causalgia)

as did the TENS parameters. Two studies recorded a statistically significant reduction in pain intensity assessed immediately after high-frequency TENS. When pain perception was assessed after the TENS protocol was complete results were mixed. After contacting the authors, they concluded that contradictory postintervention results could be explained by the differences in assessment periods. They concluded that those researchers that assessed immediately after the last session were capturing immediate results rather than short-term ones. In the negative results, delays in outcome measurement (TENS being used at home and evaluations conducted in the clinic) were the probably cause. This review also found that high-frequency TENS was more effective than low-frequency TENS.3 Dowswell and his team found that overall there was little difference in pain ratings between TENS and control groups when assessing the effect of TENS during labor. Although they did find that women receiving TENS to acupuncture points were less likely to report severe pain. Where TENS was used as an adjunct to epidural analgesia there was no evidence that it reduced pain.33

Electrical Stimulation  565

In a 2009 article in the Clinical Journal of Pain, DeSantana and colleagues used both high-frequency (100 Hz) and low-frequency (4 Hz) TENS, at strong, but comfortable sensory intensity. They were applied for 20 minutes through four electrodes placed around the surgical incision immediately after laparoscopic tubal ligation surgery (LS). They found that high- and low-frequency TENS significantly decreased postoperative pain intensity when compared with before administration of TENS. They proposed that TENS in combination with standard pharmacologic analgesic treatment was efficacious for postoperative pain relief after LS.34 But systematic reviews conducted by Robb and colleagues and Khadilkar’s team found insufficient evidence to support the use of TENS to treat cancer pain or lower back pain, respectively.35

NMES A comprehensive review of the clinical uses of NMES in 2007 found that seven of eight studies that evaluated radiographic inferior glenohumeral subluxation reported improvements. Six of seven trials found NMES had a significant effect on subluxation. But only two reported sustained improvements beyond the end of treatment.6 Glaser and colleagues found that when comparing standardized exercise therapy in conjunction with functional electrical muscle stimulation to a standardized exercise therapy alone that 4 months after the end of the electrical stimulation (during the exercise alone intervention period) the group that initially had electrical stimulation for the first 2 months of the intervention had statistically significantly improved lumbar spine function over the entire 6 months. They suggested that electrical muscle stimulation can be an effective adjunctive treatment modality for nonacute low back pain.36 Gaines when studying the effect of NMES on arthritis knee pain, found an immediate reduction in pain 15 minutes after the NMES treatment sessions but it lacked long-term improvement in pain. Renzenbrink found that when using a percutaneous NMES, there was a significant reduction in body pain and pain intensity up to 24 weeks after intervention. But other measures were not statistically significant after 24 weeks.8

IFC In a study that induced heat pain on healthy subjects to assess the tolerance created by the use of TENS and IFC found that both increased the heat pain threshold to a similar extent during stimulation but the poststimulation effect lasted longer in IFC than TENS.37 Tugay and her team found that both TENS and IFC were effective in the treatment of dysmenorrhea and were free from the potentially adverse effects of analgesics. They performed a 10-minute protocol for IFC and a 20-minute protocol for TENS. When patients were asked to assess their pain 8 hours and 8 to 24 hours after the protocol, their pain levels were below the baseline assessed immediately after the protocol. Although 8- to 24-hour measurements were increased significantly from the 8-hour assessment.5 In 2006, Walker reported that IFC, when used to treat psoriatic arthritis (PsA), improved SF-36 assessed body pain but not other SF-36 subscales. Thus, IFC had analgesic effects in PsA.37 Almeida reported in Pain that a combined ultrasound and interferential current therapy on pain and sleep in fibromyalgia led to subjective improvement of pain in terms of number and intensity of painful areas, and objective improvement with a decrease in tender point count and increased tenderness threshold. 39

Clinical Acceptance on the Market A medical device is defined, in part, as any health care product that does not achieve its primary intended purposes by chemical action or by being metabolized. There are hundreds of electrical stimulation devices that have been approved by the FDA for marketing and sale within the United States but not all devices are approved for the indication of pain management. The FDA mandates that all devices include manuals that prominently display contraindications, warnings, precautions, and adverse reactions. The Center for Devices and Radiological Health (CDRH) is the branch of the FDA responsible for the premarket approval of all medical devices. They also oversee the manufacturing, performance, and safety of these medical devices. The CDRH can require certain technical reports from the manufacturers of regulated products, or that specific radiation-emitting products meet mandatory safety performance standards, or declare regulated products defective, or order the total recall of any defective or noncompliant products on the market. Only FDA-certified devices can be lawfully sold in the United States without a medical prescription. These approved devices can be found at the corresponding FDA webpage for certified devices. All medical devices are classified according to their indication, structure, and placement by the CDRH, which assigns most electrical stimulation machines for pain management as under the medical specialty of Neurology or Physical Medicine. Because electrical stimulation is used for a number of medical conditions, any consumer interested in buying an electrical stimulation machine for the use of pain management should not only consult their primary care physician before starting a regimen but should also check to see if a device is FDA-certified and compliant for the indication of pain management.

Conclusion Electrical stimulation remains a crucial tool in the treatment of numerous acute and chronic pain conditions. Electricity throughout history has been regarded as a possible method of analgesia. Although modern medicine has not embraced it wholeheartedly, growing technologic advances have pioneered three distinct methods of the use of electrical stimulation. These widely different methods lend more weight to this growing field. And although the exact role and mechanism of how TENS, NMES, and IFC applied to the human body for analgesia has not been thoroughly established, further research may prove its benefits. Because of its wide variability, conflicting research remains to haunt this sector of medicine. Proponents of this method of pain analgesia believe that conflicting research about the extent of it efficacy in pain management is lacks consensus when it comes to the basic issues of its prescription, such as electrode placement, treatment length, and the best waveform and stimulation parameters. Clinical trials suggest that adequate dosing, particularly intensity, is critical to obtaining pain relief with electrical stimulation. Electrical stimulation is growing as a modality for pain management but continued research is needed to ensure that this technology is maximally utilized. And with this in mind, continued advancements in technology, a better understanding of optimal stimulation parameters, and a better understanding of physiologic changes induced by this technology are required.

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Studies will continue to explore these issues in the hopes of creating a universal basic protocol for electrical stimulation in modern medicine. Evidence continues to emerge from basic science and clinical trials supporting the use of electrical stimulation for the treatment of a variety of painful conditions, while identifying strategies to increase the efficacy of electrical stimulation. REFERENCES   1. Kane K, Taub A. A history of local electrical analgesia. Pain. 1975;1: 125-138.   2. Cuccurullo SJ. Electrotherapy. Physical Medicine and Rehabilitation Board Review. New York: Demos Medical; 2004: 562–567.   3. Poitras S, Brosseau L. Evidence-informed management of chronic low back pain with transcutaneous electrical nerve stimulation, interferential current, electrical muscle stimulation, ultrasound and thermotherapy. Spine J. 2008;8:226-233.   4. Khadilkar A, Odebiyi DO, Brosseau L, Wells GA. Transcutaneous electrical nerve stimulation (TENS) versus placebo for chronic low-back pain. Cochrane database of systematic reviews. 2009;2.   5. Tugay N, Akbayrak T, Demirtürk F, et al. Effectiveness of transcutaneous electrical nerve stimulation and interferential current in primary dysmenorrhea. Pain Med. 2007;8(4):295-300.   6. Sheffler LR, Chae J. Neuromuscular electrical stimulation in neurorehabilitation. Muscle Nerve. 2007;35:562-590.   7. Gaines JM, Metter EJ, Talbot LA. The effect of neuromuscular electrical stimulation on arthritis knee pain in older adults with osteoarthritis of the knee. Appl Nurs Res. 2004;17(30):201-206.   8. Mysiw WJ, Jackson RD. Electrical Stimulation. In: Braddom RL. Physical Medicine and Rehabilitation. 3rd ed. Philadelphia: WB Saunders; 2006:495.   9. Goats GC. Interferential current therapy. Br J Sports Med. 1990;24(2): 87-92. 10. Braccinano A. Transcutaneous Electrical Stimulation. Physical Agent Modalities Theory & Application for the Occupational Therapist. 2nd ed. Thorofare, NJ: Slack Inc; 2008:219-240. 11. Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965;150:971-977. 12. Melzack R, Wall P. The gate control theory of pain. In: Soulairac A, Cahn J, Carpentier J, eds. Pain: Proceedings of the International Symposium on Pain. London: Academic Press; 1968. 13. Jessel T, Kelly D. Pain and analgesia. In: Kandel E, Schwartz J, Jessel T, eds. Priniciples of Neural Science. 3rd ed. New York: Elsevier; 1991. 14. Bonica J. The Management of Pain. Malvern, Pa: Lea & Febiger; 1990. 15. Kandel E, Schwartz J, Jessel T. Principles of neural science. New York: Elsevier; 1991. 16. Allais G, De Lorenzo C, Quirico PE, et al. Non-pharmacological approaches to chronic headaches: transcutaneous electrical nerve stimulation, laser therapy and acupuncture in transformed migraine treatment. Neurological Sci. 2003;24(2 suppl):S138-S142. 17. Benedetti F. Placebo and endogenous mechanisms of analgesia. Handbook of Experimental Pharmacology. 2007;177:393-413. 18. Bjordal JM, Johnson MI, Ljunggreen AE. Transcutaneous electrical nerve stimulation (TENS) can reduce postoperative analgesic consumption. A meta-analysis with assessment of optimal treatment parameters for postoperative pain. Eur J Pain. 2003;7:181-188. 19. Goffaux P, Redmond WJ, Rainville P, Marchand S. Descending analgesia—when the spine echoes what the brain expects. Pain. 2007;130(1-2): 137-143. 20. McGaraughty S, Honore P, Wismer CT, et al. Endogenous opioid mechanisms partially mediate P2X3/P2X2/3-related antinociception in rat models of inflammatory and chemogenic pain but not neuropathic pain. Br J Pharmacol. 2005;146:180-188.

21. Washington LL, Gibson SJ, Helme RD. Age-related differences in the endogenous analgesic response to repeated cold water immersion in human volunteers. Pain. 2000;89:89-96. 22. Zhang RX, Lao L, Wang L, et al. Involvement of opioid receptors in electroacupuncture-produced anti-hyperalgesia in rats with peripheral inflammation. Brain Res. 2004;1020:12-17. 23. Barlas P, Ting SL, Chesterton LS, et al. Effects of intensity of electroacupuncture upon experimental pain in healthy human volunteers: a randomized, double-blind, placebo-controlled study. Pain. 2006;122:81-89. 24. Kawakita K, Shinbara H, Imai K, et al. How do acupuncture and moxibustion act? Focusing on the progress in Japanese acupuncture research. J Pharmacol Sci. 2006;100:443-459. 25. Fernánadez-de-Las-Peñas C, Alonso-Blanco C, Cuadrado ML, Pareja JA. Myofascial trigger points in the suboccipital muscles in episodic tension-type headache. Man Ther. 2006;11:225-230. 26. Fernándaz-de-Las-Peñas C, Cuadrado ML, Pareja JA. Myofascial trigger points, neck mobility and forward head posture in unilateral migraine. Cephalalgia: IntJ Headache. 2006;26:1061-1070. 27. Gam AN, Warming S, Larsen LH, et al. Treatment of myofascial ­trigger-points with ultrasound combined with massage and exercise— a randomised controlled trial. Pain. 1998;77:73-79. 28. Ge HY, Fernández-de-las-Peñas C, Arendt-Nielsen L. Sympathetic facilitation of hyperanalgesia evoked from myofascial tender and trigger points in patients with unilateral shoulder pain. Clin Neurophysiol. 2006;117:1545-1550. 29. Moore SR, Shurman J. Combined neuromuscular electrical stimulation and transcutaneous electrical nerve stimulation for treatment of chronic back pain: a double-blind, repeated measures comparison. Arch Phys Med Rehabil. 1997;78:55-60. 30. Renzenbrink GJ, IJzerman MJ. Percutaneous neuromuscular electrical stimulation (P-NMES) for treating shoulder pain in chronic hemiplegia. Effects on shoulder pain and quality of life. Clin Rehabil. 2004;18:359-365. 31. Yu DT, Chae J, Walker ME, et al. Comparing stimulation-induced pain during percutaneous (intramuscular) and transcutaneous neuromuscular electrical stimulation for treating shoulder subluxation in hemiplegia. Arch Phys Med Rehabil. 2001;82:756-760. 32. O’Young BJ, Young MA, Stiens SA. Physical Medicine & Rehabilitation Secrets. 3rd ed. Amsterdam: The Netherlands, Mosby; 2007. 33. Dowswell T, Bedwell C, Lavender T, Neilson JP. Transcutaneous electrical nerve stimulation (TENS) for pain relief in labour. Cochrane Database Sys Rev. 2009;2. 34. DeSantana JM, Sluka KA, Lauretti GR. High and low frequency TENS reduce postoperative pain intensity after laparoscopic tubal ligation: a randomized controlled trial. Clin J Pain. 2009;25(1):12-19. 35. Robb K, Oxberry SG, Bennett MI, et al. A cochrane systematic review of transcutaneous electrical nerve stimulation for cancer pain. J Pain Symptom Manage. 2009;37(4):746-753. 36. Glaser JA, Baltz MA, Nietert PJ, Bensen CV. Electrical muscle stimulation as an adjunct to exercise therapy in the treatment of nonacute low back pain: a randomized trial. J Pain. 2001;2(5):295-300. 37. Cheing GL, Hui-Chan CW. Analgesic effects of transcutaneous electrical nerve stimulation and interferential currents on heat pain in healthy subjects. J Rehabil Med. 2003;35:15-19. 38. Reference deleted in proofs. 39. Almeida TF, Roizenblatt S, Benedito-Silva AA, Tufik S. The effect of combined therapy (ultrasound and interferential current) on pain and sleep in fibromyalgia. Pain. 2003;104:665-672. 40. Kaplan R. Physical Medicine and Rehabilitation Review: Pearls of ­Wisdom. 2nd ed. London: McGraw-Hill/Appleton & Lange; 2005.

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Traction Gerry Catapang, PT, DPT, MGS Traction can be defined as separation of joint surfaces. The result of applied traction is distraction. Distraction means, “ to pull apart or to draw away”. Traction is a force and does not denote a change in position. Keep in mind that traction is supposed to achieve distraction.

Types of Distraction Distraction can be manual or mechanical. Manual distraction is applied via hands. Alternatively, mechanical distraction is delivers a force that can be sustained or intermittent. Manual distraction can be (1) inhibitory, (2) graded, (3) rhythmic, (4) adjustive, or (5) positional. Mechanical distraction can be three dimensional or three dimensional with autotraction. Inhibitory or inhibitive distraction is compression placed over muscles or tendons of insertion, while the joint underneath is stretched.1 An example of this is subcranial distraction. This type of distraction is based on the theory that pressure on the origin or insertion of a muscle fires the Golgi tendon apparatus (GTO) which, as a result, relaxes the muscle. With the muscles relaxed (inhibited), they do not resist the stretch being applied to the underlying joints. Graded distraction has three grades of joint play movement. The joint surfaces in grade I are nearly unweighted; grade II takes up the slack of the capsule; and grade III stretches the capsule and ligaments. Grade II is used to evaluate end feel. If the slack is taken up too early, then treatment is applied to restore joint play. Grade III is a stretch treatment. Rhythmic distraction is a series of distraction motions with alternate rest periods. With this, there is a possibility of “gating the pain”, “pumping fluids”, or both. This technique is used to decrease pain, not to increase range of motion. Adjustive distraction is a high velocity thrust often used in a joint such as the hip. The gross degree of distraction available can be determined by placing the patient supine, stabilizing one foot against the clinician’s thigh, and then applying traction on the thigh to be examined. Positional traction by Paris2 is most useful in the spine where two vertebrae are so positioned that the intervertebral foramen between them opens to relieve nerve root pressure. The patient lies over pillows and perhaps is held or assisted by straps. The three-dimensional mechanical traction table allows positioning of the patient such that the traction force results in a distraction at the spinal level and the side that is desired. The most recent traction tables are designed by Kaltenborn, Paris, and others.2

Three-dimensional mechanical autotraction allows the patient to perform traction themselves against gravity or with the assistance of a distraction table. Some traction tables can help the patient find the position of maximum comfort and allow the patient to apply the traction force.

Therapeutic Effects When performed correctly, cervical and lumbar traction can cause many effects such as distraction or separation of vertebral bodies; a combination of distraction and gliding of the facet joints; tensing of the ligamentous structures of the spinal segment; widening of the intervertebral foramen; straightening of the spinal curves; and stretching of the spinal musculature.3 Some practitioners believe fluid exchange occurs within the spinal disc during traction.4 The therapeutic efficacy of traction will be determined by the following: (1) strength of the applied force; (2) direction of the applied force; (3) position of the body; (4) state of rest or motion of the body to which the force is applied; (5) contour and texture of the body to which the force is applied; and (6) the surface on which the body rests. It is generally accepted that cervical and lumbar traction can be helpful in centralizing a pain process and in reducing radicular symptoms.5-8 Xin9 suggests that cervical traction helps with vertebrobasilar insufficiency resulting from spondylosis when combined with enhanced external counterpulsation. Others believe more definitive studies are needed to fully understand the benefits of traction.10,11

Sustained or Intermittent Mechanical Traction and Manual Traction Keep in mind that traction is a force and not a result.1 Results of sustained or intermittent mechanical traction include: (1) foraminal distraction; (2) flattening of any disc bulge; (3) relief of pressure on the nerve root. Conversely, manual traction can be sustained only for a short period of time. The techniques are often much stronger than mechanical traction techniques and the results include stretch to the myofascia; stretch to facet capsules; and occasional repositioning of vertebrae.

Clinical Studies Katavich,12 indicated in her research, that a stretch generated in cervical muscles and skin during cervical traction has the potential to influence the excitability of motor neurons. She believes manual cervical traction relieves pain and muscle spasm in the neck and 567

568  Physical Modalities for Pain Management

upper quartile. In her study, she postulated that afferent input generated by these procedures may lower the excitability of X motor neurons of upper limb muscles. Therefore, an understanding of the receptors and mechanisms underlying manual therapy may allow more effective stimulation, and hence, improved clinical outcomes. Briem,13 and others, have evaluated the immediate effects of inhibitive distraction on active range of cervical flexion in patients with neck pain. This study did not confirm the immediate effects of inhibitive distraction on cervical flexion AROM, but did provide indications for potential subgroups likely to benefit from this technique. Cai14 described positive predictors for lumbar traction to be noninvolvement of manual work, low-level fear avoidance beliefs, absence of neurologic deficits, and age >30 years. Raney15 described positive predictors for cervical traction to be when the patient reports peripheralization with lower cervical spine (C4-7) mobility testing, positive shoulder abduction test, age ≥55 years, positive upper limb tension test, and positive neck distraction test. Creighton16 confirmed the merits of positional distraction as a means to open the lumbar neuroforamen. A lateral radiograph was taken of the left lumbar neuroforamen in 10 subjects. The average foraminal opening was >4 mm at L3, L4, and L5. It is possible that even greater opening could have been achieved if towel rolls had been individually fitted—as is done in the clinical setting. Both supine and prone lumbar traction should be attempted to maximize traction benefits.17

supported. The physical therapist places the three middle fingers just caudal to the nuchal line, lifts the finger tips upward resting the hands on the treatment table, and then applies a gentle cranial pull, causing a long axis extension. The procedure is performed for 2 to 5 minutes (see Fig. 47-1).

Manual Cervical Traction Following Inhibitive Distraction The patient lies supine with head supported. The physical therapist places six finger tips, facing vertically and placed along the base of the occiput just distal to the muscular insertions but proximal to the atlas. The technique is divided into two stages: (1) the hands are drawn slightly toward the clinician until the head tilts out of the hands and rests exclusively on the finger tips (see Fig. 47-2); (2) the physical therapist now brings the front of the patient’s shoulder to contact the patient’s forehead. The patient is now held firmly between the six fingers and front of the shoulder. The physical therapist now imparts a longitudinal traction to the cervical spine (see Fig. 47-3).

Indications for Spinal Traction Clinically, traction is usually prescribed for the following conditions: (1) discogenic pain from bulges, protrusions, and herniations; (2) degenerative disc or joint disease; (3) radiculopathies; (4) facet joint syndrome; (5) joint hypomobility; (6) muscle spasms; (7) foraminal stenosis; and (8) postlaminectomy syndromes.

Contraindications for Spinal Traction Traction is known to be a safe procedure with therapeutic value in helping patients with spine-related pain. It is recommended that a detailed history, physical examination, and radiologic studies be performed prior to implementing cervical and lumbar traction techniques. Although the literature is lacking in studies reporting clear contraindications to traction, the clinician must rely on empirical information and opinion. These contraindications include (1) ligamentous instability (prior trauma or rheumatoid arthritic patients); (2) spinal infections, such as osteomyelitis, or discitis; (3) severe osteoporosis or osteopenia; (4) primary bone or spinal cord and metastatic tumors; (5) myelopathies; (6) uncontrolled hypertension or vertebral basilar artery insufficiency (for cervical traction);18 (7) the very young and the very old frail patients; and (8) acute or subacute spinal fractures. Relative contraindications for lumbar traction include pregnancy, abdominal or inguinal hernias, and aortic aneurysms.

Figure 47-1  Inhibitive cervical distraction.

Cervical Traction Techniques Inhibitive Distraction Subcranial inhibitive distraction is a myofascial technique described by Paris2 that is aimed at releasing tension in suboccipital soft tissue and suboccipital musculature. The patient lies supine with head

Figure 47-2  Manual cervical traction after inhibitive distraction, Step 1.

Traction  569

Manual Cervical Traction in Sitting Position The patient is seated on an adjustable-height table that allows the therapist to bring the patient close to the clinician. The therapist stands on a diagonal behind the patient. The arms are rested at the side of the patient’s mastoid processes and the palms of the hand are cupped (see Fig. 47-4). The clinician leans back, keeping the

hands at a constant height from the floor. Traction is applied due to the increasing distance between the mastoids that are moving backwards, and the ischial tuberosities that are remaining stable (see Fig. 47-5).

Positional Cervical Distraction Patient is instructed to lie supine. Patient is then instructed to raise head and neck until slack of forward bending is removed form the level to be distracted. Head is supported (e.g., on a firm stack of books). The radial border of one hand forms a fulcrum that is placed opposite the foramen to be opened. The neck is then bent over the hand. Static or intermittent traction may now be applied (see Fig. 47-6). Patient can try following through with this technique at home for 20 minutes twice a day.

Over-the-Door Cervical Traction (Fig. 47-7) Preparing for Treatment Instruct the patient to sit on a chair (not on a stool). Position the neck at 20 to 30 degrees of forward flexion. This angle of vertical pull is an important factor to straighten the normal cervical lordosis, as well as to keep the foramina at its widest diameter. Figure 47-3  Manual cervical traction after inhibitive distraction, Step 2.

Position the chair so the rope in front of the patient’s head is in the exact center.

Figure 47-4  Manual cervical traction in sitting position, Step 1.

Figure 47-5  Manual cervical traction in sitting position, Step 2.

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Applying Traction Explain the procedure to the patient. Inform the patient that the sensation to be experienced is one of a gentle pull without producing any increase in pain. Any nausea or dizziness is not normal. Any numbness of sensory changes that may occur is also not normal. Warn the patient not to move the chair or body. The patient should be sitting in a relaxed position with feet resting on the floor or a foot stool, the back against the back rest and the arms resting on arm rests or patient’s sides.

Figure 47-6  Positional cervical distraction.

Put the halter on the patient. In case the patient is wearing dentures, these need to be removed and replaced by a thick gauze pad between the gums. Wig, earrings, and eyeglasses should also be removed. The chin and occipital areas of the halter should be padded with gauze to avoid direct pressure and for hygienic reasons. Connect the halter to the spreader bar and have the patient put the water bag on lap. Take up the slack in the rope and recheck the angle of pull as well as the pressure points. Allow the bag to descend gradually and let it hang to produce the traction. The treatment time is usually 20 to 30 minutes. Disconnect the halter and check the patient.

Mechanical Traction (Saunders Cervical Traction) Preparing for Treatment Place the traction unit on a carpeted floor or other firm surface. Check to make sure that the air hose is not being pinched by the extension loop or bottom of the unit. Make sure you have enough room to lie down in a comfortable position. Separate the neck wedges by rotating either of the black adjustment knobs so that your neck fits easily between the wedges. You can make additional adjustments after you lie down in the traction unit. Loosen the hook and loop adjustable head strap; center the head strap sleeve with the seam side “up”. Move the head pad down on the neck carriage track as far as it will go, by rotating the gauge housing to the “release” position. Place the pump in a position so that you can reach it during treatment. Position the shoulder pad over the extension loop. Set a timer for the length of treatment. Figure 47-7  Over-the-door cervical traction.

Set the patient facing the traction unit. This is the best position. Be sure the head halter and strap are safe and clean. Fill the bag with water (10 to 40 pounds are usually sufficient). The maximum of 30 lb for females and smaller males and 40 lb for muscular males is suggested. The patient will be able to tolerate only the minimum amount of traction initially (this amount can be gradually increased).

Applying the Traction Lie down on your back, positioning your body so the neck wedges cradle your neck and your head rests comfortably on the head pad. The neck wedges should contact your neck midway between the tips of your earlobes and the top of your shoulders. Turn either of the black adjustment knobs until the wedges have moved firmly against both sides of the neck. As you settle into the traction unit, the neck wedges may slightly rotate and self-adjust to the contour of your head and neck, or you can rotate the wedges manually as needed for the most comfortable fit.

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Figure 47-9  Lumbar positional distraction.

Figure 47-8  Mechanical traction (Saunders Cervical Traction).

To ensure proper positioning, scoot down so the neck wedges firmly contact the base of your skull. Secure the headstrap sleeve, seam side up, over your forehead using the hook and loop attachment. This strap should fit snugly. Apply traction using the pump as described in the user’s manual. The desired number of pounds for the cervical area is anywhere between 10 to 40 lb. The desired treatment time, is around 20 to 30 minutes. Comply with the instructions and progression provided by the therapist (see Fig. 47-8). Figure 47-10  Mechanical traction (Saunders Lumbar Traction).

Lumbar Traction Techniques Positional Distraction To facilitate lumbar positional distraction, the following steps are followed14: (1) a firm bolster is made up of pillow and sheet and placed at the level of iliac crest; (2) the bolster is placed opposite the level at which maximum side-bending is desired; (3) both legs are then bent forward at the hip and knees to bring the opening to desired level; (4) the spine is now rotated at the level above where the maximal opening is desired; (5) the patient is now in positional distraction (see Fig. 47-9); (6) a belt may be added to help maintain the position. Initially, treatment time is not more than 5 minutes on the first day. Gradually increase the treatment duration in 5- to 10-minute increments until a 40-minute regimen is attained.

Mechanical Traction (Saunders Lumbar Traction) Preparing for Treatment Place the Saunders Lumbar Traction device in its case on a firm surface or bed with the wheels facing up. Remove the wheels and unzip the case. Open the case lid toward the head of the bed or treatment surface. Remove the hand pump from the mesh storage compartment. Place the hand pump next to the device. Open the buckles on each of the harnesses. Position the lower harness so it is slightly overlapping the upper harness. Have a clock, timer, or wrist watch available to time your treatment.

Applying Traction Lie down on the Saunders Lumbar Traction device so that the lower harness is 1 inch over the top of your hips. If desired, or as instructed by your physical therapist, place pillows, wedges, or bolsters under your knees, back, and/or head. Secure the lower harness over you bare skin first. Tighten the belts as snugly as possible without pain. Now secure the upper harness the same way. Apply traction using the pump as described in the user’s manual. The desired number of pounds for the lumbar area is any point between 50 to 150 lb. The desired treatment time is around 20 to 30 minutes. Comply with the instructions and progression provided by physical therapist (see Fig. 47-10).

Amount of Force to Produce Spinal Traction In the lumbar spine, it has been reported that 120 lb for 15 minutes is necessary to produce a structural change (movement) at the spinal segment.3 A force equal to one-half of the patient’s body weight on a friction-free surface is thought to be a minimum to cause therapeutic effects in the lumbar spine.3 However, a therapeutic effect may occur with less than one half of the body weight. Therefore, it is important to document patient’s reaction and results of treatment per visit. Adjustments can be made to achieve maximum results. In the cervical spine, it has been shown that 25 to 45 lb forces were necessary to demonstrate a measurable change in the posterior

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cervical spine structures and separation of the intervertebral discs.3 Changes at the atlantooccipital and atlantoaxial joints with 10 lb of traction have been noted.3 Less force appears necessary to produce separation in the upper cervical spine. Ligamentous rupture in the lumbar spine has been described in cadaveric studies with 880 lb of force, thoracolumbar spine with 400 lb of force, and 120 lb in cervical spine (disc rupture).3

Treatment Adjuncts to Increase Therapeutic Efficacy of Traction Hot moist packs, ultrasound, soft tissue mobilization, and muscle stretching will help the muscles relax prior to cervical or lumbar traction. After traction, cryotherapy and interferential treatment may help reduce pain and swelling.

Conclusion Traction is a helpful technique to relieve pain and muscle spasm in the neck and low back. Clinical studies indicate that traction helps in the centralization of pain and the reduction of extremity symptoms such as tingling and numbness. Incorporation of other physical modalities may increase the therapeutic efficacy of traction. REFERENCES   1. Paris SVP. S3 Seminar Manual Cervical Evaluation and Manipulation. 4th ed. St. Augustine, Fla. Paris, Inc; 2000: 94.   2. Paris SVP. S1 Seminar Manual Extremity Evaluation and Manipulation. 2nd ed. St. Augustine, Fla: Institute of Graduate Physical Therapy; 1991, 99, 197.   3. Saunders HD, Saunders R. Evaluation, Treatment, and Prevention of Musculoskeletal Disorders. 3rd ed. Chaska, Minn: Educational Opportunities; 1995: 281–289, 298. 3a. Catapang GP. Tracking the causes of chronic pain. Advance for Directors in Rehabilitation. June 2008:57. 3b. Huang ZJ, Chen JX, Qi WW. Clinical research on treatment of vertebroarterial type of cervical spondylosis with 5 step manipulation and traction. J Tradit Chin Med. 2009;29(4):268-270. 3c. Paris SVP, Loubert PV. Foundations of Clincial Orthopedics. 3rd ed. St. Augustine, Fla: Institute Press; 1999, 342.

  4. Cholewicki J, Lee AS, Reeves NP, Calle EA. Trunk muscle response to various protocols of lumbar traction. Man Ther. 2009;14(5):562-566.   5. Jellad A, Ben Salah Z, Boudokhane S, et al. The value of intermittent cervical traction in recent cervical radiculopathy. Ann Phys Rehabil Med. 2009;52(9):638-652.   6. Moeti P, Marcheti G. Clinical outcome from mechanical intermittent cervical traction for the treatment of cervical radiculopathy: A case series. J Orthop Sports Phys Ther. 2001;31(4):207-213.   7. Olivero WC, Dulebohn SC. Results of halter cervical traction for the treatment of cervical radiculopathy; retrospective review of 81 patients. Neurosurg Focus. 2002 Feb 15;12(2).   8. Swezey RL, Swezey AM, Warner K. Efficacy of home cervical traction therapy. Am J Phys Med Rehabil. 1999;78(1):30-32.   9. Xin W, Fangjian G, Hua W, et al. Enhanced external counterpulsation and traction therapy ameliorates rotational vertebral artery flow insufficiency resulting from cervical spondylosis. Spine. 2010;35:1415-1422. 10. Graham N, Gross AR, Goldsmith C. Mechanical traction for ­mechanical neck disorders: A systematic review. J Rehabil Med. 2006; 38(3):145-152. 11. Graham N, Gross A, Goldsmith, et al. Mechanical traction for neck pain with or without radiculopathy. Cochrane Database Syst Rev. 2008;16(3):CD006408. 12. Katavich L. Neural mechanisms underlying manual cervical traction. J Orthop ManipTher. 1999;7(1):20-25. 13. Briem K, Huijbregts P. Thorseteinsdottir M. Immediate effects of inhibitive distraction on active range of cervical flexion in patients with neck pain: A pilot study. J Man Manip Ther. 2007;15:82-92. 14. Cai C, Pua YH, Lim KC. A clinical prediction rule for classifying patients with low back pain who demonstrate short-term improvement with mechanical lumbar traction. Eur Spine J. 2009;18(4):554-561. 15. Raney NH, Petersen EJ, Smith TA, et al. Development of a clinical prediction rule to identify patients with neck pain likely to benefit from cervical traction and exercise. Eur Spine J. 2009;18(3):382-391. 16. Creighton D. Positional distraction, a radiological confirmation. J Orthop Manip Ther. 1993;1(3):83-86. 17. Beattie PF, Nelson RM, Michener LA, et al. Outcomes after a prone lumbar traction protocol for patients with activity-limiting low back pain: A prospective case series study. Arch Phys Med Rehabil. 2008; 89(2):269-274. 18. Reyes T. Introduction to Physical Therapy and Patient Care, Hyrotherapy, Traction, and Massage. 2nd ed. Manila, Philippines: UST Press; 1985:121.

48

Manual Therapy Peter A. Huijbregts, PT, MSc, MHSc, DPT, OCS, FAAOMPT, FCAMT

Certainly many of our patients equate manual therapy exclusively with the manipulative thrust or high-velocity, low-amplitude (HVLA) maneuver practiced by clinicians in the diverse professions of physical therapy, medicine, chiropractic, osteopathy, naprapathy, traditional Chinese medicine, and naturopathy as part of their legislated scope of practice. However, manual therapy, in fact, also encompasses a great variety of other techniques. The American Physical Therapy Association (APTA) has defined manual therapy techniques as “skilled hand movements intended to improve tissue extensibility, increase range of motion, induce relaxation, mobilize or manipulate soft tissue and joints, modulate pain, and reduce soft tissue swelling, inflammation, or restriction”. Techniques matched with these proposed indications for manual therapy include massage, manual lymphatic drainage, manual traction, mobilization/ manipulation, and passive range of motion (ROM).1 Although within physical therapy in the United States, defined synonymously as “a manual therapy technique comprised of a continuum of skilled passive movements to joints and/or related soft tissues that are applied at varying speeds and amplitudes, including a small amplitude/high velocity therapeutic movement”, more commonly the term manipulation is used to describe a thrust technique performed at a pathologic end of range of a joint, whereas mobilization describes a nonthrust, sustained or oscillatory, low-velocity movement within or at the end of range of joint motion.1 Additional specified manual therapy interventions include soft tissue and neural mobilization, joint stabilization, and self-mobilization exercises.2 The goal of this chapter is to introduce the reader to manual therapy interventions and approaches used for patient management within physical therapy. Various manual techniques have been developed within osteopathy including muscle-energy, straincounterstrain, and craniosacral osteopathy, and the reader is referred for a discussion of these techniques to the chapter in this text on osteopathic medicine. Information on various soft tissue mobilization techniques can likewise also be found in the chapter on bodywork and movement therapies and manual ­traction is mostly discussed in the chapter on traction. In this chapter we will first review the history of manual therapy as an introduction to the various present-day approaches within physical therapy and then discuss proposed mechanisms of action and examination and diagnosis within manual therapy. The chapter concludes with a discussion of proposed indications for manual therapy combined with a review of outcome studies followed by a review of proposed contraindications linked to evidence of risk of harm to allow the reader to

make informed decisions with regard to manual therapy management based on current best evidence.

History of Manual Therapy Early Medicine Manual therapy is among the oldest recorded interventions in medicine. Documentation of its practice dates back over 4000 years to Egyptian scrolls (Edwin Smith papyrus) and its use was also depicted in ancient Thai sculptures.3 The first mention of massage appears in the Nei Ching, the oldest existing medical work, dedicated to the Chinese Emperor Huang Ti in 2598 bc. Ancient Indian and Greek texts, including the work of ­Hippocrates, describe massage as an effective therapy for treating injuries resulting from war or sports.4 Hippocrates (460-385 bc) also described a combination of traction and manipulation on the back of a patient lying prone on a wooden bed in his treatise, On Setting Joints by Leverage.5 Whether Hippocrates solely attempted by this method to reposition traumatically displaced vertebrae or if he intended to manipulate slightly luxated vertebrae for a variety of indications, to this day remains a matter of debate.6 The Roman physician Galen (131 to 202) commented on Hippocrates’ techniques in 18 of his 97 surviving treatises, as did the influential Arabic physician Abu Ali ibn Sina, better known as Avicenna (980 to 1037). In 1656, Friar Thomas described manipulative techniques for the extremities in his book, The Complete Bone Setter, and in as late as 1674, Johannes Scultetus still included descriptions of Hippocrates’ manipulative methods in his text, The Surgeon’s Storehouse.7 Manipulation fell out of favor in medicine when Sir Percival Pott (1714 to 1788) described tuberculosis of the spine and condemned traction and manipulation as not only useless but dangerous.5-7 However, manipulation in the form of bone setting continued to be practiced with some of its lay practitioners attaining great notoriety including Sarah Mapp in 18th century and Sir Albert Baker in 20th century England, who both counted royalty among their patients. In the United States, the male members of the Rhode Island Sweet family were reputed to possess hereditary skills in bone setting. One of them, Waterman Sweet, in 1829 published a text called, An Essay on the Science of Bone Setting. Bone setting continues to be practiced today in large parts of the world by lay practitioners as a form of folk medicine.8 573

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During this time, manual therapy in medicine was relegated to a number of fringe clinicians, foremost among them the 1784 Edinburgh University graduate Edward Harrison. Harrison published in the London Medical and Physical Journal on a proposed pathophysiologic connection between spinal subluxations and visceral disease and adjusted vertebrae by pressing on the spinous or transverse processes with his thumbs or with a device.5,6,9 In 1828, Glasgow physician, Thomas Brown, popularized in the medical community the concept of “spinal irritation”. Brown proposed that a shared nerve supply could implicate the spine in visceral disease and nervous conditions, which led him to target the spine with nonmanipulative heroic medicine interventions including local blistering, application of leeches, and cautery. Dr. Isaac Parrish of Philadelphia introduced the concept of spinal irritation in North America with an article on the topic in The American Journal of Medical Sciences.9,10 Riadore, a prominent London physician practicing manipulation, stated in 1842, “if an organ is insufficiently supplied with nervous energy or blood, its function is decreased and sooner or later its structure becomes endangered.5 With their theories acceptable even to many eminent 19th century medical physicians, it is easy to understand how first osteopathy after 1874 and then chiropractic after 1895 and its offshoots, naturopathy after 1902 and naprapathy after 1905, rapidly gained widespread acceptance among the American general population.

Early Physical Therapy Meanwhile, there was also renewed interest from the medical community in manual therapy. In 1867, the British Medical Journal reported on a lecture by Dr. James Paget, On the Cases that Bonesetters Cure. In 1871, Dr. Wharton Hood wrote a series complementary to bone setting for the Lancet based on his experiences with a bone setter named Hutton, and in 1882 there was a discussion of bone setting at the 50th annual meeting of the British Medical Association.5,7 One reason for this renewed interest might have been the influx and successful establishment of thriving practices by the earliest Swedish-educated physical therapists in various countries, including the United Kingdom. Physical therapy as a governmentsanctioned, university-educated profession began when, in 1813, in Stockholm Pehr Hendrik Ling (1776 to 1839) founded the ­Kungliga Gymnastiska Centralinstitutet or Royal Central Institute for Gymnastics (RCIG) in Stockholm.11 Students at the RCIG were either noblemen or belonged to the upper echelons of society; most were also army officers. They were instructed in physical education, military gymnastics (mainly fencing), and physical therapy or medical gymnastics. The medical gymnastics taught and practiced included a strong manual therapy component, leading Ottoson12 to describe physical therapy as the world’s oldest manual therapy profession (Figs. 48-1 to 48-3). Although, by today’s standards, the manual therapy component instructed in Ling’s system can hardly be called segment specific, clinicians educated at the RCIG certainly further developed and published more specific manipulative interventions.13 Empowered by their scientific training and propelled by an unwavering conviction that physical therapy could positively affect many conditions including (and thereby not unlike osteopathy and chiropractic) a multitude of nonmusculoskeletal pathologies, RCIG graduates traveled around the globe to disseminate their approach to patient management based on what they considered current best evidence. As early as the 1830s they started establishing clinics in

Figure 48-1  Lumbar mobilization ad modem Ling. (Reproduced with kind permission from Dr. Anders Ottoson, National Archives of Sweden, http://www.chronomedica.se).

many European cities. A great number of foreign doctors and laymen traveled to Stockholm to study physical therapy with Ling’s successor Lars Gabriel Branding (1799 to 1881). Meanwhile in Sweden, an 80-year turf war erupted between these early physical therapists and the fledgling orthopedic medicine specialization, from which the orthopedic physicians at the Karolinska Institute eventually emerged victorious.11,14 Physical therapy education in Sweden and eventually worldwide was restructured to a technical education producing allied health technicians. In English-language countries, physical therapy was often practiced by nurses with additional course work in massage and exercise therapy. In other Western European countries, physical education teachers with additional course work in rehabilitative exercise, often begrudgingly gave up their previous professional independence for support from the medical profession in their search for societal recognition.15 In rapid succession, national associations arose from these physical therapy technicians. In 1889 in the Netherlands, physical therapists founded the world’s first professional association, the Society for Practising Heilgymnastics in the Netherlands. In 1894, in Great Britain, the Society of Trained Masseuses was founded and in 1906 in Australia, the Australasian Massage Association.15,16 Physical therapy in the United States had a relatively late start with the founding of the American Women’s Physical Therapeutic Association in 1921. When the United States entered World War I, it did not, in contrast to its European allies, have a military with an established division of physical therapy. By command of the Surgeon General, a number of university physical education programs,

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Figure 48-3  Temporomandibular joint mobilization ad modem Ling. ­(Reproduced with kind permission from Dr. Anders Ottoson, National Archives of Sweden, http://www.chronomedica.se).

Figure 48-2  Thoracic traction ad modem Ling. (Reproduced with kind permission from Dr. Anders Ottoson, National Archives of Sweden, http://www.chronomedica.se).

instituted physiotherapy “War Emergency Courses” to train women who could physically rehabilitate returning soldiers. As a result, 90% of World War I physical therapists came from schools of physical education; in fact, the physician then in charge of the Army Physiotherapy Division stipulated that all therapists have 4-year university degrees in physical education in addition to their physical therapy training. When in 1922 the military reduced therapy services as a result of government cutbacks, many therapists previously employed by the military were forced into the private sector. This led to conflicts with other manual medicine practitioners including nurses, osteopaths, and chiropractors all claiming to practice physical therapy. It was this early conflict especially with the chiropractic profession that caused therapists to align themselves more closely with medical physicians. To garner physician support, U.S. physical therapists in 1930 voluntary relinquished their right to see patients without physician referral.17 In the United States, this close alliance with the medical profession and the adversarial relationship between physicians, and especially chiropractors, also had physical therapists in their communication with physicians deemphasize the use of manual therapy in their clinical practice—although these interventions continued to be used and further developed within the profession

with various publications during this period in the U.S. professional physical therapy literature.18 In Western Europe and Scandinavia, this adversarial stance never developed. Instead, medical physicians embraced osteopathy, chiropractic, and other manual medicine approaches indigenous to Europe. Throughout Europe, postgraduate manual medicine training institutes were well attended by physicians and even academic chairs in manual medicine were established.19 These European physicians also educated their physical therapy technicians in manual therapy. Dr. James Mennell (1880 to 1957), the medical officer at St. Thomas Hospital in London, taught manipulation to physical therapists as of 1916. His son, Dr. John McMillan Mennell (1916 to 1992) educated physicians and physical therapists worldwide in manipulation and, with Dr. Janet Travell, cofounded the North American Academy of Manipulative Medicine. Dr. James Henry Cyriax (1904 to 1985), Mennell’s successor at St. Thomas, stated that physical therapists were the most apt professionals to learn manipulative techniques. Mennell is most known for developing and instructing therapists and physicians worldwide. His system of orthopedic medicine emphasized clinical diagnosis and conservative management by way of mainly friction massage, exercise, manipulation, and infiltration. Less well known is his link to early Swedish physical therapy, although his father (Dr. Edgar Cyriax 1874 to 1955), and his maternal grandfather (Jonas Henrik Kellgren 1837 to 1916), were both RCIG graduates. Another influential person teaching manipulation to therapists at this time at the London School of Osteopathy was Dr. Allan Stoddard, qualified in medicine and osteopathy. Therapists and physicians were also educated in manual therapy at the British School of Osteopathy as of 1920.7

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Manual Therapy Approaches Kaltenborn-Evjenth Approach Without a doubt the most important person to again increase the emphasis on manual therapy within the profession of physical therapy was Norwegian-born Freddy Kaltenborn (1928-). Already trained as a physical education teacher he was admitted as the first male student to the Norwegian program in physical therapy in 1948. Educated in London in orthopedic medicine by Dr. James Cyriax from 1952 to 1954 and qualifying in chiropractic in Germany in 1958 and in osteopathy at the London School of Osteopathy with Dr. Stoddard in 1962, Kaltenborn -from 1968 on associated with physical therapist Olav Evjenth—developed an eclectic manual therapy system known as the Kaltenborn-Evjenth approach.14 With Kaltenborn the first clinician to apply the new science of arthrokinematics to manual therapy,7 central to the Kaltenborn-Evjenth approach is the emphasis on restoration of the gliding component of a normal joint roll-gliding movement. Also central is the concept of a treatment plane defined as the plane across the concave joint surface. With manual translatoric techniques defined in this system as encompassing traction, compression, and gliding techniques, traction and compression are performed perpendicular to this treatment plane, whereas gliding techniques induce movement parallel to this plane. Mobilization and manipulation techniques are used to reduce pain and increase ROM. Joint restrictions are classified as periarticular, articular, intraarticular, or combined in etiology. Periarticular restrictions owing to adaptive shortening of neuromuscular and inert structures (including skin, retinacula, and scar tissue) and articular structures (capsule and ligaments) are treated with sustained mobilization techniques, whereas periarticular restriction due to arthrogenic muscle hypertonicity is managed with neurophysiologic inhibitory techniques including thrust techniques.20 Intraarticular restrictions are best treated with (traction) manipulation initiated from the actual resting position.21

Maitland (Australian) Approach In Australia, physical therapist Geoff Maitland (1924-) after studying abroad with Cyriax and Stoddard and physical therapists Gregory Grieve and Jennifer Hickling developed his own approach and started teaching a manual therapy system at the University of ­Adelaide in the entry-level physical therapy program. The world’s first 3-month certificate program was offered in 1965. In 1974, 12-month postgraduate diploma courses in manipulative therapy were offered at physical therapy programs in Australia. This approach to manual therapy is now referred to as the ­Maitland or Australian approach.22 Although it is often associated with variations of the nonthrust posteroanterior pressure technique (Fig. 48-4), the Maitland system uses a whole spectrum of thrust and nonthrust techniques. Perhaps its greatest contribution is its emphasis on structured clinical reasoning. History-taking is used to gather information that is used in the subsequent physical examination to establish the patient’s concordant or comparable signs. A concordant sign consists of pain or other symptoms reproduced on physical examination that are indicated by the patient as a chief complaint or reason to seek therapy.23 A thorough history-taking allows the clinician to distinguish between concordant and discordant signs. Discordant signs are findings on physical examination seemingly implicating a source of symptoms that are, however, in

Figure 48-4  Lumbar posteroanterior mobilization: Oscillating mobilization is applied through straight arms with pisiform bone of one hand reinforced by other hand contacting dorsal tip spinous process.

no way related to the chief complaint.24 Unique to the Maitland approach are also the frequent immediate postintervention reevaluations of the deemed most relevant concordant or so-called asterisk signs to guide further management.

Paris Approach In 1960, physical therapist Stanley Paris from New Zealand received a scholarship from the New Zealand Workers Compensation Board to study with Freddy Kaltenborn and Allan Stoddard. On his return to New Zealand, he organized courses and introduced, among others, later influential physical therapists Robin McKenzie and Brian Mulligan to manual therapy before leaving to teach and practice in the United States. Paris became the voice of manual therapy as a specialization within orthopedic physical therapy within the United States and worldwide. Denied access—for being a physical therapist and not a physician—to the North American Academy of Manipulative Medicine by Dr. Janet Travell, he founded the North American Academy of Manipulative Therapy in 1968, which was disbanded in 1974 to become the Manual Therapy Special Interest Group in Canada and the Orthopedic Section of the APTA in the United States. Together with, among others, physical therapists Grieve, Kaltenborn, Lamb, and Maitland, Paris also founded in Montreal in 1974, the International Federation of Orthopaedic Manipulative Therapists (IFOMT), the first recognized subgroup of the World Confederation of Physical Therapy. At the urging of Kaltenborn, Paris was again involved in 1991 in organizing the American Academy of Orthopedic Manual Therapy.5,7,14 Most relevant to U.S. physicians referring for manual therapy is that fellows in this organization (designated FAAOMPT) have demonstrated advanced proficiency in manual therapy skills and knowledge. Paris also developed an eclectic system of manual therapy. In addition to

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a unique diagnostic classification system, and central to this system, is the emphasis not on addressing pain but on treating dysfunction defined as a state of altered mechanics, either an increase or decrease from the expected normal, or the presence of an aberrant motion.25

Mechanical Diagnosis and Therapy: McKenzie Approach Although emphasizing patient independence by way of specific exercise self-treatment, physical therapist Robin McKenzie of New Zealand has developed a strongly research-based approach to management of spinal and extremity conditions called the McKenzie or Mechanical Diagnosis and Therapy (MDT) approach that incorporates examination and treatment by way of sustained and repeated movements and, if required, mostly nonthrust manual therapy interventions. Classification into postural, dysfunction, or derangement syndromes is guided by patient report of pain during repeated movement examination occurring within range or at end range and by the possible occurrence of centralization and peripheralization. Unique to the MDT concept and indicative of the derangement syndrome—strongly associated in the spine with discogenic ­dysfunction—centralization is defined as “the situation in which pain arising from the spine and felt laterally from the midline or distally is reduced and transferred to a more central or near midline position when certain movements are performed”. Peripheralization describes the opposite condition, whereby movements cause pain to be felt more distally or laterally from the midline.26

Mulligan Approach New Zealand physical therapist Brian Mulligan suggested minor positional faults as an etiology for joint dysfunction thought to respond to a unique manual therapy intervention called mobilizations with movement (MWM).27 With an MWM, the therapist applies a sustained accessory glide, long-axis rotation, or combination while the patient actively performs a previously, but now no longer painful, movement (Fig. 48-5). The Mulligan approach shares with the Kaltenborn approach an emphasis on restoration of the gliding component of the normal joint roll-gliding movement.28 Central to both is also the concept of the treatment plane but, whereas Kaltenborn emphasizes gliding techniques in the direction normally associated with the restricted physiologic motion, Mulligan often starts with a sustained glide at a right angle to this physiologic glide. An iterative process then tests glides in different directions or long-axis rotation before settling on the most effective direction allowing for pain-free active ROM or isometric muscle contraction, together constituting the MWM.28,29 Although ­Mulligan’s NAGs or natural apophyseal glides, mid to end-range facet joint mobilizations applied anterosuperiorly along the treatment plane, are perhaps less unique, the SNAGs or sustained natural apophyseal glides that combine active movement with therapist-applied mobilization certainly are. The techniques are supported by a home program of self-mobilization and corrective taping.27

Neural Mobilization Based to a large extent on pioneering work by Breig,30 ­Australian physical therapists Robert Elvey, David Butler, and Michael Shacklock have contributed greatly to our understanding of the possible role of impaired neural mobility in the etiology of

Figure 48-5  Mobilization with movement for lateral epicondylalgia.

neuromusculoskeletal dysfunction.31,32 Also used in diagnosis, interventional neural mobilization techniques attempt to restore normal neural mobility or neurodynamic function in relation to the structures surrounding the nerve by inducing stretch or tension in the affected nerves or by mobilizing the surrounding tissues (Fig. 48-6).2 Butler has more recently expanded on this approach by integrating new insights with regard to pain physiology.33

Other Manual Therapy Systems: Canadian, Grimsby, and Dutch Approaches Other manual therapy systems relevant mostly to North ­America include eclectic systems such as the Grimsby, Canadian, and Dutch manual therapy approaches. The Grimsby approach developed by Norwegian physical therapist Ola Grimsby and the Canadian approach initially developed by Canadian and English physical therapists David Lamb, Erl Pettman, Cliff Fowler, Jim Meadows, Ann Hoke, and Diane Lee are derived mainly from the Kaltenborn-Evjenth approach but continue to be developed into progressively more distinct systems of diagnosis and management.34-39 Most characteristic of the Grimsby approach is its emphasis on very specific exercise progressions. The Canadian approach (and its U.S. counterpart instructed at the North American Institute of Orthopaedic Manual Therapy or NAIOMT) emphasizes the use of screening examinations to guide further examination and diagnosis. The Dutch manual therapy system40 combines various manual therapy approaches developed within medicine, physical therapy, chiropractic, and osteopathy and bases diagnosis and management greatly on assumptions with regard to three-dimensional motion behavior of joints and on extrapolations related to somato-somatic and somato-autonomic neuroanatomic connections.

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Figure 48-7  Assisted soft tissue mobilization (ASTYM) treatment for lateral epicondylalgia. (Reproduced with kind permission from Dr. Tom Sevier, www.astym.com).

Figure 48-6  Upper limb nerve tension test (ULNTT 1) median bias: Sequential combination of shoulder girdle depression, shoulder abduction and external rotation, elbow extension and supination, wrist and finger extension, and thumb abduction and extension.

Massage and Soft-Tissue Mobilization Although often erroneously associated with Pehr Hendrik Ling, Swedish massage was again popularized in the late 19th century as a viable medical treatment by Dr. Johan Georg Mezger (1838 to 1909), a Dutch physical education teacher turned physician.15 Also called traditional or —when applied to athletes—sports massage,41 most therapists do not consider Swedish massage a systematic manual therapy approach but rather a preparatory modality consisting of effleurage or rhythmic stroking hand movements, petrissage or kneading, tapotement or manual percussive massage, friction or deep penetrating pressure delivered through the finger tips, and vibration or shaking.4 James Cyriax promoted deep friction massage transverse to the fiber direction for the treatment of ligament and tendon injuries3 and from this various instrumented-assisted versions have developed including most prominently Graston technique and ASTYM (assisted soft tissue mobilization). The ASTYM method was developed by sports physician Dr. Tom Sevier, who not only has taken great care to investigate and support the method with basic and applied research evidence but who has also created a national outcome database to help therapists establish a research-based prognosis. Unlike Graston technique, initially marketed by Dr. Sevier’s former instrument maker, Mr. Dave Graston, ASTYM is not simply an instrumentassisted locally applied cross friction technique but is used to treat the whole kinetic chain involved with established protocols that are adapted by the clinician based on patient presentation (Fig. 48-7).

As do bodywork therapists, physical therapists also use softtissue mobilization, which includes techniques intended to affect muscles and connective tissues such as stretching, myofascial release, trigger point techniques, and deep tissue techniques.2 Myofascial release and deep tissue techniques are discussed in more detail in the chapter on bodywork and movement therapies. Active release technique (ART) is a form of deep tissue technique developed by the chiropractor P. Michael Leahy. In ART, protocols based on symptom patterns are linked to manual treatment of specific anatomic sites. Specific techniques are then used for release of proposed soft tissue adhesions that consist of applying deep digital tension, usually with the thumb or two fingers combined with both active and passive passage of the tissue through this area of deep tension. An active home stretching program follows this manual treatment.42 Stretching techniques performed by therapists in the context of manual therapy intervention can take the form of static or facilitated stretching. In the 1950s, physical therapists Margaret Knott & Dorothy Voss43 developed proprioceptive neuromuscular facilitation (PNF) that by way of a combination of isometric contractions and mid through end range movements in three-dimensional naturally occurring spiral and diagonal patterns used reflexogenic activation and relaxation for specific stretching, strengthening, and stabilization. Postisometric relaxation is a European manual medicine technique similar to a PNF hold-relax-stretch technique in that the patient is asked to gently contract a muscle from a slightly lengthened position followed by a further gentle stretch on relaxation.44 Manual trigger point therapy is an intervention often used in physical therapy. In the late 1930s, Dr. Janet Travell, at that time a cardiologist and medical researcher, became interested in muscle pain. In the early 1960s, physiatrist Dr. David Simons and his wife, physical therapist Lois Simons, started collaborating with Travell, which eventually resulted in the Trigger Point Manuals, consisting of two volumes on the upper and the lower half of the body.45,46 Although initially, in addition to spray-and-stretch techniques, heavy ischemic pressure was advocated as a manual technique for treatment of myofascial trigger points, the updated second edition of the first volume instead suggested the use of gentle digital pressure or trigger point pressure release.47

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Physical therapists sometimes use other systems of massage and soft tissue mobilization that propose effects beyond those solely on the neuromusculoskeletal system. Those include, but are not limited to, Japanese Shiatsu acupressure massage, connective tissue massage, and Rolfing.48,49 Acupressure massage uses a rationale for management choices that is consistent with that used for acupuncture in traditional Chinese medicine. Connective tissue massage was developed by German physical therapists Elisabeth Dicke and Hede Teirich-Leube and physician W. Kohlrausch. In 1929, Dicke had serious endarteritis obliterans and amputation of her leg was considered. Noticing an increased tension in the skin and subcutaneous tissue of her lumbosacral region, she attempted to reduce the discomfort there by applying a stroking massage. She not only noted a sharp local sensation, but also itching and a feeling of warmth spreading into her affected leg. Continued selftreatment resulted in improvement of her ischemic complaints. Connective tissue massage is a reflex therapy that uses a manually applied shear force at connective tissue interfaces in the skin. This has been proposed to stimulate autonomic nerve endings, thereby restoring balance between the sympathetic and parasympathetic components of the autonomic nervous system. By way of cutaneovisceral responses evoked in segmentally related skin areas, this form of massage has also been hypothesized to affect internal organ function.49-51 Manual lymphatic drainage is a light-touch massage technique combined with patient education and compressive garments developed in the 1930s in France by the Danish psychologist Dr. Emil Vodder. It is primarily intended to have an effect on soft tissue edema.52

Joint Stabilization and Specific Exercise Although inadequate joint stability is mostly addressed in physical therapy by way of a patient-specific home exercise program, manual techniques can also be used to produce somatosensory feedback when the goal is to produce appropriate muscular activity. Specific self-mobilization exercises are modeled on joint and soft tissue assessment and mobilization techniques that are often unique to the various manual therapy approaches to patient management.

Proposed Mechanisms of Action By its very nature it would seem plausible that manual therapy has mechanical and neurophysiologic effects. In addition, the careful examination inherent in most manual therapy approaches, the manual identification and thereby confirmation by the clinician of the patient’s complaint, and the manual contact involving patient consent and cooperation during subsequent treatment is likely to also produce therapeutic psychological effects.

Mechanical Effects Although it is not possible to separate mechanical and neurophysiologic effects in clinical research, disruption of articular and/or periarticular adhesions, release of entrapped synovial folds or plicae, reduction of displaced nuclear fragments, and unbuckling of motion segments have all been suggested as mechanical effects of thrust techniques.53 Peak force magnitudes used during spinal thrust techniques easily exceed body weight and are attained within 100 to 200 msec.54 Increased strain rates with thrust techniques lead to increased stiffness in collagenous tissues, possibly resulting in failure or disruption of adhesions with decreased joint excursion

when compared to low-velocity techniques. Alternatively, mobility restrictions owing to collagenous shortening, fibrosis, or hyperplasia would likely benefit more from the viscoelastic deformation produced by sustained or oscillatory nonthrust articular and soft tissue techniques.53 The synovial fluid is composed of 15% suspended gases, 80% of which is carbon dioxide and the rest mainly oxygen and nitrogen. Thrust techniques cause a rapid distraction of the joint cavity resulting in a similarly rapid drop by some 3.5 atmosphere in intraarticular pressure. Although the joint will unsuccessfully try to adapt with invagination of capsular tissue into the joint cavity, the sudden local reduction of pressure will cause a process called cavitation whereby the previously suspended gases are released from solution and form a gas bubble within the joint. The cavitation process itself or the subsequent collapse of this gas bubble is what causes the audible release that often accompanies thrust techniques.55 Manipulation of a joint is followed by a refractory period of some 15 to 30 minutes during which the gas is again reabsorbed into the synovial fluid and no new cavitation can be produced.56 The joint distention due to the presence of nonsuspended gases in the synovial fluid during this period has been hypothesized to result in viscoelastic deformation of restricted capsuloligamentous structures.57 Although the traction component of thrust techniques seems a plausible mechanism for unbuckling or restoring appropriate alignment of displaced joint partners, research has not supported this proposed mechanism.53 Similarly, research so far has also failed to support the minor positional fault mechanism postulated by ­Mulligan.29 Evans53 suggested that release of entrapped synovial folds or inclusions is also unlikely and proposed neurophysiologic effects on persistent associated muscle spasm after such a mechanical event had occurred and spontaneously resolved. Cyriax58 suggested that manipulation might restore displaced nuclear fragments to a more central location within the intervertebral disc (IVD). However, although various case reports have described positive effects of thrust techniques on carefully selected patients with IVD lesions,59 others have suggested that positive outcomes may be more related to natural history than to a mechanical effect of the manipulation. In fact, manipulation of a segment with a disc affected by trauma or degeneration, especially a noncontained herniation where the outer annulus is compromised, might lead to further injury, extrusion, and progressive neurologic compromise.60 In contrast to the equivocal mechanical effects of thrust techniques of the IVD and as initially proposed by McKenzie26 as a mechanical explanation for the effect of repeated movements, research on asymptomatic human subjects does show movement of the nucleus of the lumbar IVD anteriorly with extension and posteriorly with flexion in nondegenerated discs.60 Although research on symptomatic subjects is limited, Donelson and coworkers61 have shown the ability to differentiate with repeated movement testing between patients with a competent and noncompetent outer annulus suggesting similar mechanical effects in degenerated discs. Friction massage has been hypothesized to stimulate tissue healing by way of local mechanical effects. Research has indeed shown cellular responses in the sense of increased fibroblast recruitment and activation and mechanical responses indicative of accelerated tissue healing with instrument-assisted deep friction massage.62-64 Swedish or sports massage has been hypothesized— although it is unclear whether this effect is mediated mechanically or neurophysiologically—to affect muscle tissue healing and recovery. However, a review on this topic showed limited and conflicting evidence for effects of massage on muscle blood flow and indicated

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that an effect of massage on lactate clearance was unlikely. Massage did result in significant decreases in delayed-onset muscle soreness (DOMS) but again, the evidence for an increased rate of postDOMS force recovery—possibly indicative of accelerated muscle repair processes due to massage—was limited. There was also insufficient evidence for the effects of massage on recovery from muscle fatigue, although a trend was noted for endurance more so than strength performance.41

Neurophysiologic Effects To this day, in some approaches to manual therapy, mechanical explanations for the mechanism of action of manual therapy interventions are considered more relevant than neurophysiologic explanations. However, the firmly held convictions that clinicians are able to apply segment-specific interventions and that such specific interventions are always required for optimal patient outcome, have not been supported by the available research. Segmental specificity is a biomechanical impossibility when applying the central posteroanterior pressures associated with the Maitland system. In the lumbar spine, for example, posteroanterior pressures resulted in motion of the entire lumbar region,65,66 whereas in the cervical spine, the same technique produced minimal, if any, intervertebral motion when applied at C2 or C6.67 Beffa and Mathews68 noted an equal distribution of cavitation induced from the sacroiliac to the L3-4 joints with thrust techniques aimed at either the sacroiliac or the L5-S1 joints. Ross and associates69 noted that manipulation of the lumbar and thoracic spine produced cavitation at the targeted joint only about 50% of the time; however, most procedures resulted in multiple cavitations, thereby including the target segment. Reggars70 showed that a thrust technique directed at C3-4 resulted in multiple-level cavitations in 82% of subjects, showing the lack of segmental specificity also for this cervical technique. With regard to the need for specificity of the manual therapy technique for optimal results, Chiradejnant and colleagues71 noted no between-group differences on any of the outcome measures used in a group of patients with low back pain (LBP), who were treated with either unilateral or central posteroanterior or transverse pressures that had been selected by the therapist based on examination findings or randomly generated. In a case series, ­Cleland and colleagues72 noted favorable outcomes in patients who fit a prediction rule for sacroiliac joint manipulation in LBP, even though they were treated with a rotational technique aimed at the lumbar spine. Van Schalkwyk and Parkin-Smith73 found no between-group postintervention differences in patients with mechanical neck pain and segmental restriction when using either a rotational or lateral break manipulation technique. In their systematic review of randomized controlled trials investigating manual therapy for patients with nonspecific LBP, Kent and associates74 noted that studies in which the clinician was not given the choice of treatment technique actually had better short-term outcomes with regard to pain and activity limitation than those studies in which the clinicians were given a treatment choice; long-term outcomes were equal in both types of studies. Haas and colleagues75 showed that there were no short-term between-group differences in pain and stiffness ratings when patients with neck pain were manipulated at a segment with decreased segmental mobility or at a randomly generated segment. Although this research evidence in no way disproves the notion that for some patients specific manual therapy interventions will, in fact, provide better outcomes, it does indicate the need for all clinicians

to more seriously consider possible neurophysiologic mechanisms of action for manual therapy interventions. Input for neurophysiologic effects of manual therapy likely occurs by stimulation of cutaneous, musculotendinous, and capsuloligamentous receptors. Stimulation of thick fiber afferent neurons might explain analgesia by way of activation of the gate control mechanism postulated by Melzack and Wall.76 The persistent postcavitation distention of the joint capsule has been hypothesized to cause depolarization of the thick fiber afferent type III articular mechanoreceptors with resultant inhibitory effects on periarticular muscles.57 Massage has been shown to reduce motor neuron excitability as measured by a decreased H-reflex in both neurologically normal subjects and in subjects with spinal cord injury.77-79 Although Herzog54 suggested this was due to an artifact related to positional changes, manipulation research has produced similar decreases in motor neuron excitability in healthy subjects that were even more pronounced in subjects with chronic pain.2 Of course, we cannot exclude supraspinal influences as causing or contributing to this decreased motor neuron excitability but, considering the seemingly increased motor neuron excitability related to those higher-level systems discussed subsequently, this reduction in excitability would seem caused by segmental mechanisms. Because of the synaptic connections between low-threshold joint and muscle mechanoreceptors, the dorsal periaqueductal gray (PAG) area of the midbrain may also have a role in manipulationinduced analgesia by way of descending inhibitory mechanisms. This PAG plays an important integrative role with regard to the response to stress, pain, and other stimuli by coordination of the nociceptive, autonomic, and motor systems. Its hypothesized role has been supported by manipulation studies showing sympathoexcitation and central postmanipulation motor facilitation—the latter also evidenced by muscle activation remote from the area of manipulation occurring some 50 to 200 msecs after manipulation.54,80,81 The ventrolateral PAG exerts its descending inhibitory influence by way of an opioid mechanism but research has been equivocal when it has come to detecting elevated plasma beta-endorphin levels after manipulation or massage. Similarly, intravenously administered opioid antagonists have not been shown to reverse the hypoalgesic effect of at least nonthrust manual therapy interventions.82 Although one can question relevance of plasma samples to extrapolate regarding the central role of endorphins in manipulation-induced analgesia with endorphins too large to penetrate the blood-brain barrier, recently the endocannabinoid system has been suggested as relevant to the analgesic but also mood-enhancing effects of manual therapy interventions.83,84 Animal research has also indicated a role for the neuropeptide oxytocin in the plasma and in the PAG in the analgesia produced by massage. Blockade of the oxytocin receptors either in the PAG or systemically was shown to reduce the analgesic effects of massage. Massage in human subjects has been shown to decrease cortisol and increase serotonin levels.2 Animal research also has implicated central mechanisms working by way of serotonin and norepinephrine in the analgesia produced by nonthrust joint mobilization but no role for gamma-aminobutyric acid (GABA) or endogenous opioids.85

Psychological Effects Massage has also been shown to have significant positive effects on mood states including depression and anxiety in various patient populations.86-90 Whether this is a psychological effect or whether it is mediated by endogenous opioid or endocannabinoid, actions

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related to descending inhibitory systems is unclear. For thrust techniques, the occurrence of an audible release due to cavitation has been suggested as relevant to the patient experiencing a psychological therapeutic effect.57 Preliminary evidence, however, suggests that occurrence or nonoccurrence of this phenomenon has no effect on the short-term outcome with regard to pain, function, or ROM in patients with mechanical LBP91 or neck pain92 and on 4-week outcomes in patients with LBP.93

Examination and Diagnosis Manual Therapy Examination As noted above, within manual therapy there are various distinct approaches to patient management. The specific information that a clinician looks for, the order in which it is obtained, and the emphasis that is given to the data collected, varies depending on the approach to manual therapy used. However, as with a normal orthopedic examination data are collected from history-taking and physical examination. Data from imaging and other medical diagnostic studies—are used if available and requested from the medical provider involved or—depending on the legislation governing physical therapy scope of practice—ordered by the therapist were deemed relevant. The clinical physical examination consists of standard orthopedic tests including observation, active and passive ROM examination, manual muscle tests, neuroconductive and neurodynamic tests, orthopedic special tests, and palpation. Although thoroughly integrated even within physical therapy entry-level education, positional and specific tissue palpation, joint play tests, motion palpation tests, and certain provocation tests might be considered tests specific to manual therapy. Even though research has generally not shown these tests to be reliable or valid,94 positional palpation tests to establish the presence of possible malposition related to joint dysfunction are still advocated and used within some manual therapy approaches. Palpation for changes in tissue texture thought to be indicative of segmental dysfunction have shown some interrater reliability but abnormalities are found in symptomatic and asymptomatic subjects indicating likely limited diagnostic value. Joint play tests assess for ROM, symptom reproduction, resistance through range and at end range (the latter also known as end feel), and overall impression during passive accessory motion testing of the extremity joints. Various types of motion palpation tests (Table 48-1) assess for similar qualities in the spine and sacroiliac joints (Figs. 48-8 and 48-9). Intrarater agreement for isolated spinal motion palpation tests varies from less than chance to generally moderate or substantial agreement, whereas interrater agreement only rarely exceeds poor to fair agreement. Rating scales for mobility are less reliable than rating for pain. Given the neurophysiologic mechanisms of action described for manual therapy and the lack of a need, in at least some patients, for segmental specificity of the manual therapy intervention, knowing there is a joint dysfunction may be more relevant than knowing the exact location and direction of the dysfunction. Thus, even less reliable tests might provide appropriate guidance for manual therapy management.95 In contrast to data on isolated tests, pragmatic combinations of various motion palpation tests left to clinician discretion have shown high predictive validity for pain relief with zygapophyseal infiltrations in the cervical and lumbar spine.96,97 Provocation tests have more consistently demonstrated sufficient reliability and diagnostic accuracy.94 Laslett and coworkers23

Table 48-1  Types of Spinal Motion Palpation Type of ­Palpation

Description

Active motion palpation

Assessment technique in which the clinician palpates bony landmarks while guiding the patient through cardinal plane motions of the trunk

Passive motion palpation

Assessment technique whereby one vertebra is moved in physiologic ranges on another (PPIVM) Assessment technique whereby ­segmental mobility is assessed through the translatory motions associated with physiologic motions (PAIVM) PAIVM tests that specifically test for accessory motions that should not or minimally be present in a normal motion segment (PAIVM)

PAIVM, passive accessory intervertebral motion palpation; PPIVM, passive physiological­ intervertebral motion palpation.

Figure 48-8  Passive physiologic intervertebral motion (PPIVM) test for segmental lumbar flexion.

studied concurrent criterion-related validity of a comprehensive examination consisting of an MDT repeated movement evaluation combined with a cluster of SIJ provocation tests including the distraction, compression, thigh thrust, pelvic torsion, and sacral thrust tests. The rating scale for the individual tests was dichotomous; the subjects were diagnosed with SIJD when three or more tests were positive after exclusion of discogenic complaints with the repeated movement evaluation. The gold standard test was a fluoroscopically guided double SIJ block with at least 80% pain reduction. The authors reported positive LR of 6.97 (95% CI 2.70 to 20.27) and a negative LR of 0.11 (95% CI 0.02 to 0.44). Excluding the discogenic patients yielded a positive LR of 4.16 (95% CI 2.16 to 8.39) and a negative LR of 0.12 (95% CI 0.02 to 0.49). Acknowledging the relevance of clusters of tests rather than isolated tests in clinical reasoning and patient management, recent research within manual therapy has emphasized the development

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and validation of clinical prediction rules. Clinical prediction rules (CPR) are decision-making tools that contain predictor variables obtained from patient history, examination, and simple diagnostic tests; they can assist in making a diagnosis, establishing prognosis, or determining appropriate management.98 As Childs and Flynn99 pointed out, if studies included in a systematic review or metaanalysis use no patient classification other than the broad category of nonspecific low back (or neck) pain, the resultant heterogeneous study samples likely preclude finding real effects of any intervention. CPR research is one method to identify a more homogeneous diagnostic subgroup of patients that is expected to respond to manual therapy intervention. Relevant CPRs are discussed under treatment-based diagnostic classification.

Diagnostic Classification in Manual Therapy Findings from the history and physical examination (and possibly data from imaging and additional medical diagnostic data) are evaluated to establish a manual therapy diagnosis. Diagnosis is classification of patients based on predetermined defining characteristics and as such, diagnosis requires a classification system that, to be useful for manual therapy diagnosis within physical therapy, must meet the following criteria1: The system must be consistent with boundaries placed on the profession by law or society. ll The tests necessary for confirming the diagnosis must be within the legal purview of physical therapy. ll The label used to categorize a condition must direct the selection of interventions toward those interventions that are part of the physical therapy scope of practice. ll

Classification systems are clinimetric indices: rating scales and other expressions are used to measure symptoms, physical signs, and other phenomena in clinical medicine. Clinimetric indices relevant to classification systems used for manual therapy diagnosis include status indices, prognostic indices, clinical guideline indices, and mixed indices.100

Status and Mixed Indices Status indices are classification systems used to define patient problems. The most common clinically used example is the International Classification of Diseases (ICD), a taxonomy of diagnostic labels for the purpose of standardizing nomenclature of diagnoses for statistical and administrative reasons. Because the ICD-manual does not describe the procedures used to apply the diagnostic labels, reliability of assigning ICD-9 codes is low.100 The traditional medical, structure-based model is also a status index: It assumes a direct correlation between underlying pathology and signs and symptoms and uses a pathoanatomic classification system.101 Indicating its limited value to manual therapy diagnosis, the structure-based medical model is unable to provide up to 85% of patients with LBP with a specific diagnosis owing to the weak association between symptoms, pathologic changes, and results from imaging tests.102,103 Still, manual therapy diagnosis, at times, does use this structure-based or pathoanatomic model. Diagnostic labels include facet joint syndrome, sacroiliac joint syndrome, and disc lesions. The classifications developed by the “Quebec Task Forces on Spinal Disorders and on Whiplash-Associated Disorders” are mixed indices, designed to help make clinical decisions, establish prognosis, and evaluate the quality of care for patients with low back pain or whiplash injuries.100

Prognostic Indices A prognostic index allows the clinician to predict rehabilitation potential and is intended to aid in making decisions on referral for other services and/or manual therapy management. Research into the predictive validity of (clusters of ) signs and symptoms is required to produce prognostic indices. By way of example of prognostic indices relevant to manual therapy management, Jull and ­Stanton104 identified patients with cervicogenic headache, who did or did not achieve a 50% to 79% or 80% to 100% reduction in headache immediately and 12 months postintervention. Only the absence of lightheadedness indicated higher odds of achieving either a 50% to 79% (OR = 5.45) or 80% to 100% (OR = 5.7) reduction in long-term headache frequency. As noted earlier, Donelson and associates61 established the prognostic validity of the centralization phenomenon with repeated movement examination in the management of patients with discogenic LBP. Hancock and colleagues105 identified three predictor variables for recovery in patients with mechanical LBP receiving spinal manual therapy and diclofenac. Of patients with baseline pain ≤ 7/10, (and) duration of the current episode ≤ 5 days, and number of previous episodes ≤ 1, 60% can be expected to recover (defined as 0 to 1 pain level on 0 to 10 pain scale for 7 days) at 1 week, whereas 95% will recover at 12 weeks.

Clinical Guideline Indices: Mechanism and Treatment-Based Classification Figure 48-9  Passive physiologic intervertebral motion (PPIVM) test for segmental unilateral cervical extension.

A clinical guideline index is a diagnostic classification system designed specifically to provide instructions on treatment. Most relevant to manual therapy diagnosis are the mechanism- and

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treatment-based classification systems. The mechanism-based classification system is based on the premise that dysfunctions identified during examination are the cause of pain and decreased function.106 The intent of mechanism-based manual therapy diagnosis is to identify the joint(s) and/or soft tissues implicated, the extent of damage to the tissue, the possible neuroreflexive extension of the local impairment, and the levels of reactivity and ability for a targeted or selective response to intervention within the nervous system.40 In the treatment-based system, a cluster of signs and symptoms from the patient history and physical examination ideally derived from CPR or other relevant research is used to classify

patients into subgroups with specific implications for management. In manual therapy, the once predominant mechanismbased system is increasingly supplemented by treatment-based classification systems. The most extensively researched treatmentbased classification systems are the MDT approach as proposed by McKenzie and the treatment-based classification system for patients with neck pain and LBP originated at the University of Pittsburgh presented in Tables 48-2 and 48-3.107-110 Vicenzino and colleagues111 have provided preliminary suggestions for a treatment-based classification system for patients with lateral epicondylalgia.

Table 48-2  Treatment-Based Classification for Patients with Neck Pain Classification

Examination Findings

Mobility

ll ll ll ll

Centralization

ll ll ll ll

Conditioning and increased exercise tolerance

ll ll ll ll

Pain control

ll ll ll ll ll

Reduce headache

ll ll ll

Recent onset of symptoms No radicular or referred symptoms in the upper quarter Restricted range of motion with rotation and/or discrepancy in side-bending No signs of nerve root compression or peripheralization of symptoms in the upper quarter with cervical range of motion Radicular or referred symptoms in the upper quarter Peripheralization and/or centralization of symptoms with range of motion Signs of nerve root compression present May have pathoanatomic diagnosis of cervical radiculopathy Lower pain and disability scores Longer duration of symptoms No signs of nerve root compromise No peripheralization and/or centralization of symptoms with range of motion High pain and disability scores Very recent onset of symptoms Symptoms precipitated by trauma Referred or radiating symptoms extending into the upper quarter Poor tolerance for examination or most interventions Unilateral headache with onset preceded by neck pain Headache pain triggered by neck movement or positions Headache pain elicited by pressure on posterior neck

Proposed Matched Interventions ll

ll

ll ll

ll

ll

ll ll ll ll

ll ll ll

Cervical and thoracic spine mobilization and/or manipulation Active range of motion exercises

Mechanical and/or manual traction Repeated movements to centralize symptoms

Strengthening and endurance exercises for the muscles of the neck and upper quarter Aerobic conditioning exercises

Gentle active range of motion within pain tolerance Range of motion exercises for adjacent regions Physical modalities as needed Activity modification to control pain Cervical spine mobilization and/or manipulation Strengthening of the neck and upper quadrant muscles Postural education

Table 48-3  Treatment-Based Classification for Patients with Low Back Pain Classification

Examination Findings

Specific exercise

ll ll ll

Stabilization

ll ll ll ll ll ll ll

Manipulation

ll ll ll ll

Traction

ll ll ll

Strong preference for sitting or walking Centralization with motion testing Peripheralization in direction opposite centralization Younger age Increased straight-leg raise range of motion Aberrant motions present Positive prone instability test Hypermobility with spring testing Increasing episode frequency Three or more previous episodes More recent onset of symptoms No symptoms distal to the knee FABQ Work scale score < 19 Hypomobility with lumbar spring testing Leg symptoms Signs of nerve root compression Peripheralization with extension movements and/or positive crossed straight-leg raise

Proposed Matched Interventions ll

Repeated endrange exercises

ll

Trunk strengthening and stabilization exercises

ll

Manual therapy Range of motion exercise

ll

Traction intervention and repeated endrange exercise

ll

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584  Physical Modalities for Pain Management

Clinical Prediction Rules Various CPRs have been produced related to management within the treatment-based classification system for patients with neck pain and low back pain discussed previously. Flynn and associates112 developed a clinical prediction rule consisting of five predictor criteria to identify a subgroup of patients with nonspecific LBP, who were likely to benefit from thrust manipulation (Fig. 48-10). This rule was subsequently validated by Childs and colleagues,113 who calculated an adjusted OR of 114.7 at the 1-week follow-up and one of 60.8 for a positive functional outcome at the 4-week follow-up for patients who were positive on the rule (≥ 4 predictor criteria present) and received manipulation versus those patients who were negative on the rule and received exercise. Fritz and coworkers114 derived a subsequent 2-factor rule from this prediction rule and reported a positive LR of 7.2 for a positive outcome in patients with LBP who were positive on both predictor variables and treated with manipulation. Fritz and associates115 reported preliminary evidence that there is a subgroup of patients with LBP likely to benefit from traction characterized by leg symptoms, signs of nerve root compression, and peripheralization with extension movements or a positive crossed straight-leg raise test. Hicks and colleagues116 identified four variables relevant to predicting success with stabilization exercises for patients with LBP: age < 40, average straight-leg raise test > 91(o), presence of aberrant motions, and a positive prone instability test (Fig. 48-11). The presence of three or more variables indicated the greatest likelihood of success with a positive LR of 4.0 (95% CI 1.6 to 10.0). Variables associated with failure were negative prone instability test, absence of aberrant motions, absence of hypermobility on lumbar spring testing, and a Fear Avoidance Beliefs Questionnaire Physical Activity (FABQ-PA) subscale score of < 9. Two or more of these variables present carried a negative LR of 0.18 (95% CI 0.08 to 0.38). Similarly, Fritz and colleagues117 identified longer symptom duration, symptoms in the leg or buttock, absence of lumbar hypomobility, less hip rotation ROM, less side-toside discrepancy in hip internal rotation ROM, and a negative pelvic torsion test as predictors of lack of success with manipulation. Tseng and associates118 identified six predictor variables for an immediate positive response to cervical manipulation (­Fig. 48-12)

Figure 48-10  Sacroiliac thrust manipulation as used in lumbar manipulation derivation and validation clinical prediction rule studies112,113: lumbar spine is protected by locking into extension-rotation and thrust is delivered to anterior superior iliac spine imparting posterior innominate rotation.

in patients with neck pain including patients diagnosed with cervical spondylosis with or without radiculopathy, cervical herniated disc, myofascial pain syndrome, and cervicogenic headache. An increasing number of predictor variables present led to progressively higher positive likelihood ratios of an immediate positive

Figure 48-11  Prone instability test: pain reproduced with central posteroanterior pressure with feet on the ground is abolished or reduced when lifting both feet off the ground; this manipulation contracts the lumbar extensor muscles.

Figure 48-12  Cervical unilateral flexion thrust manipulation: Lower ­cervical spine is protected with ligamentous tension by flexion up to the level to be manipulated, while the end range at the segment is engaged by a ­combination of ipsilateral side-bending, contralateral rotation, and ­contralateral side-gliding; the cervical spine cranial to the segment that is manipulated is held in a neutral position.

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response to manipulation: four predictor variables present yielded an LR of 5.33 and an 89% probability of a successful manipulation. Cleland and colleagues119 derived six predictor variables in patients with mechanical neck pain without neurologic involvement, indicating a likely positive response to a combination of three different thoracic thrust manipulations (Fig. 48-13 and 48-14), one simple

cervical ROM exercise, and patient education. They suggested using a criterion of three of six variables present as a sufficient research-based indication for the use of thoracic manipulation in patients with mechanical neck pain: three of six variables present yielded a positive LR of 5.5 and an 86% probability of a successful outcome. Raney and coworkers120 developed a five-factor CPR for response to cervical traction and exercise and reported a positive LR of 4.8 (95% CI 2.2 to 11.4) for the patient reporting a great deal of improvement if three or more predictor variables were present. Table 48-4 provides the predictor variables in the various manual therapy-related CPRs. CPRs have also been developed although not validated, related to the use of manual therapy in patients with lateral epicondylalgia, patellofemoral syndrome, knee osteoarthritis, chronic tension-type headache, shoulder pain, and ankle inversion sprain.121-126 For a review of relevant clinical prediction rules, the reader is referred to Glynn and Weisbach.127

Table 48-4  Clinical Prediction Rules/Predictor Variables CPR to Identify Patients with LBP Most Likely to Benefit from Manipulation ll ll ll ll ll

Duration of current episode < 16 days No symptoms distal to the knee FABQW score < 19 ≥ 1 hypomobile segment on lumbar segmental mobility testing One or both hips with > 35 degrees of internal rotation range of motion (ROM)

Abbreviated CPR to Identify Patients with LBP Most Likely to ­Benefit from Manipulation ll ll

Figure 48-13  Seated upper thoracic traction manipulation: The neck is ­protected by locking the hands of the therapist around it and the ­midthoracic spine is locked and protected with a combination of extension and muscular tension. Traction manipulation can be applied segmentally or more regionally.

Duration of current episode less < 16 days No symptoms distal to the knee

CPR to Identify Patients with Immediate Response to Cervical Manipulation ll ll ll ll ll ll

Initial NDI < 11.50 Bilateral involvement pattern Not performing sedentary work > 5 hours per day Feeling better while moving the neck Not feeling worse when extending the neck Diagnosis of spondylosis without radiculopathy

CPR to Identify Patients with Neck Pain Likely to Respond to ­Thoracic Manipulation ll ll ll ll ll ll

Symptom duration < 30 days No symptoms distal to the shoulder Looking up does not aggravate symptoms FABQPA score < 12 Diminished upper thoracic kyphosis Cervical extension range of motion < 30 degrees

CPR to Identify Patients Likely to Benefit from Cervical Traction and Exercise ll ll ll ll

ll

Figure 48-14  Midthoracic traction manipulation: Traction forces are localized by hand fixation on the caudal vertebra of the motion segment and by flexion (possibly combined with side-bending toward and rotation away from the therapist) of the spine cranial to the segment to be manipulated.

Age ≥ 55 Positive shoulder abduction test Positive median bias upper limb nerve tension test Symptoms peripheralize with central posteroanterior testing   at C4-7 Positive neck distraction test

CPR, clinical prediction rule; FABQPA, Fear Avoidance Beliefs Questionnaire Physical Activity Subscale; FABQW, Fear Avoidance Beliefs Questionnaire Work Subscale; LBP, low back pain; NDI, Neck Disability Index.

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Indications and Outcomes Research Indications

both statistically and clinically significant improvements in pain and function.

Cervicogenic Dizziness therapy1

The APTA definition of manual provided in the introduction to this chapter comprehensively discusses the most common indications for manual therapy interventions within physical therapy. Unlike indications for manual therapy found in, for example, contemporary chiropractic and osteopathy, all of these indications concern neuromusculoskeletal dysfunction. In North America, connective tissue massage is most frequently used for orthopedic problems; however, indications are also suggested for cardiac and respiratory diseases, peripheral circulatory deficits, neurologic pathologies, gynecologic and obstetric problems, and disorders of the digestive system and urinary tract.50,51 Indications suggested for the other less mainstream forms of massage including acupressure massage likewise may extend beyond the neuromusculoskeletal realm. The clinician should keep in mind that all these common indications were developed based mostly on the proposed mechanisms of action for manual therapy interventions discussed earlier. In the era of evidence-informed clinical practice, such extrapolations and assumptions based on scientific evidence need to be supplemented by clinical outcome studies available for the various interventions.

Mechanical Neck Pain Relevant to the management of patients with mechanical neck pain, in a systematic review Ezzo and associates128 noted that all (quasi) randomized trials included had studied multimodal interventions and that, therefore, the sole effectiveness of massage for patients with mechanical neck pain remained unknown. Systematic reviews on the effectiveness of manual therapy for mechanical neck pain have indicated positive outcomes on pain and function for (non) thrust interventions only when combined with exercise and only in subacute and chronic conditions.129,130 Hoving and colleagues131 reported no significant between-group differences for pain, perceived recovery, and function in patients with neck pain managed by their family physician, exercise and stretching, or nonthrust techniques, and stabilization exercises at 1 year but they noted short-term effectiveness significantly improved for the manual therapy group at 7 weeks. Further indicating the cost-­ effectiveness of manual therapy management for patients with mechanical neck pain, an economic evaluation alongside this randomized controlled trial (RCT) also showed significantly lower cost for the manual therapy intervention when compared to both other therapies.132 Consistent with the CPR research discussed earlier,119 a meta-analysis showed significant short-term improvements with thoracic thrust manipulation with regard to neck pain, disability, and cervical ROM in specific subgroups.133 A systematic review identified one RCT on the use of the MDT approach for patients with neck pain that showed similar results to exercise therapy.134 Suggesting an indication for manual therapy intervention also in patients with cervical radiculopathy, in a multicenter RCT, Young and colleagues135 studied the effect of true versus sham mechanical traction for cervical radiculopathy. Although they found no between-group differences for pain and function, both groups also received cervical and thoracic nonthrust techniques, thoracic thrust techniques, postural education, and cervical mobility and cervical and scapulothoracic strengthening exercises resulting in

A systematic review of randomized and noncontrolled clinical trials found consistent significant improvements with soft tissue, nonthrust, and thrust interventions for patients with cervicogenic dizziness.136 A subsequent RCT in patients with cervicogenic dizziness treated with a Mulligan cervical SNAG intervention showed clinically and statistically significant reduced dizziness, neck pain, and dizziness-related disability over the group treated with detuned laser.137

Headache A systematic review noted moderate evidence for short-term efficacy of spinal manipulation similar to amitriptyline in patients with migraine and chronic tension-type headache, whereas there was no added benefit if manipulation was added to massage in patients with episodic tension-type headache.138. Bronfort and associates138 also reported moderate evidence that spinal manipulation was more effective for cervicogenic headache than was massage. A systematic review yielded two RCTs that showed significant effects of spinal thrust interventions on headache intensity and duration and medication intake in patients with cervicogenic headache.139 Another systematic review concluded that there was limited evidence for massage and connective tissue mobilization in patients with ­tension-type headache, whereas the evidence for spinal manipulation, manual traction, and craniosacral therapy was inconclusive.140 An RCT showed that twice weekly 45-minute massage and trigger point release sessions resulted in significant decreases in headache frequency, intensity, and duration and headache-related disability in patients with tension-type headache with these effects lasting into the 3-week follow-up period.141 Fernandez-de-las-Penas and colleagues122 developed a CPR to identify patients with chronic tension-type headache, who might benefit from manual trigger point therapy consisting of varied combinations of pressure release, muscle energy, and soft tissue techniques combined with progressive, low-load deep cervical flexor and extensor muscle strengthening exercises. Relevant improvement was defined as an at least 50% reduction in either headache intensity, frequency, or duration and an increase of ≥ 5 points on a 15-point global rating of change or patient satisfaction scale. Four variables predicted benefit at 1 week after discharge: headache duration < 8.5 hours per day, headache frequency < 5.5 days per week, Short Form-36 bodily pain domain score < 47, and SF36 vitality domain score < 47.5. With three variables present, the positive LR was 3.4 (95% CI 1.4 to 8.0). With all four present, the positive LR increased to 5.9 (95% CI 0.8 to 42.9). Two variables predicted benefit one month postdischarge: headache frequency < 5.5 days per week and SF36 bodily pain domain score < 47. With one variable present, the positive LR was 2.2 (95% CI 1.2 to 3.8); two variables present yielded a positive LR of 4.6 (95% CI 1.2 to 17.9). Although migraine headache might seem to present less of an indication for manual intervention, a prospective cohort study showed significant improvements in headache frequency, intensity, duration, and disability after 2 months of thrust interventions as indicated by the clinician to the whole spine; at 12 months there were still significant improvements when compared to baseline for headache frequency, intensity, and duration and medication use.142 An RCT comparing spinal manipulation to interferential

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current showed significant between-group differences favoring manipulation for headache frequency, duration, disability, and medication use during the 2-month postintervention follow-up in patients with migraine headache.143

Temporomandibular Dysfunction A systematic review of RCTs144 reported significant between-group differences favoring manual therapy combined with exercise over occlusal splint therapy with regard to pain and mouth opening range in patients with arthrogenous temporomandibular dysfunction owing to an anteriorly displaced intraarticular disc. A systematic review including randomized and nonrandomized trials145 showed immediate postintervention effects of manual therapy on mouth opening and reduction in periarticular EMG signals; multiple cohort designs with up to 6 months’ follow-up showed significant effects on pain, mouth opening, and perceived recovery with a multimodal program including active exercise, postural correction, relaxation training, hot pack application, and manual therapy. Kalamir and coworkers146 reported that cervical manipulation might be beneficial for patients with temporomandibular disorders, although this recommendation was based solely on case studies.

Thoracic Dysfunction Aspegren and associates147 noted in a case report that Graston technique and thrust techniques to the thoracic spine and ribs might be of benefit to patients with acute costochondritis. However, and indicating the lack of research effort in this area, a systematic review found no research evidence from RCTs for the effect of thoracic manipulation on thoracic spine conditions.133

Mechanical Low-Back Pain In their systematic review of randomized trials, Furlan and colleagues148 noted that massage (and most notably acupressuretype massage) was beneficial with regard to pain and function in patients with mechanical LBP for up to 1 year postintervention. Effects improved if massage was combined with exercise and patient education. Hammer and Pfefer,149 reported on the use of Graston technique in a patient with a clinical diagnosis of subacute lumbar compartment syndrome. Older systematic reviews and meta-analyses noted either no evidence that spinal manipulation was superior to other therapies for patients with acute or chronic LBP;150 insufficient evidence for superior outcomes over physical therapy without manipulative interventions, exercise, or medical care in patients with subacute LBP;151 or statistically (but likely not clinically significant) superior outcomes over placebo or nonsteroidal antiinflammatory medication in patients with chronic LBP.152 Insufficiently homogeneous study samples likely have impaired our ability to detect a true effect of manipulation and more recent CPR research into identifying treatment-based subgroups of patients with mechanical LBP. Further indicating the importance of reliable subclassification, a systematic review of RCTs noted that the MDT approach for patients with LBP resulted in greater short-term reductions in pain and disability when compared to “standard” treatments.134 With regard to manual therapy interventions in patients with lumbar spinal stenosis, Reinman and colleagues153 reviewed randomized, cohort, and case studies and series and reported potential benefit of mainly nonthrust interventions to the lumbar and thoracic spine, pelvis, and lower extremities. With regard to

cost-effectiveness, at the 6-month follow-up in the manipulation CPR validation study, patients who had received manipulation had significantly lower health care utilization, medication use, and time off from work due to LBP than those receiving exercise only.113 Similarly, the UK BEAM trial that compared medical management to manipulation or manipulation combined with exercise showed that manipulation or manipulation combined with exercise was the most cost-effective approach to the management of patients with mechanical LBP.154

Shoulder Dysfunction Massage has been shown to result in significant improvements over wait list controls with regard to pain, function, and ROM in patients with shoulder pain.155 In a case report, Hammer156 described the use of Graston technique in a patient with supraspinatus tendinopathy. A systematic review of RCTs noted limited evidence to support thoracic manipulation for shoulder problems.133 However, cohort studies have shown immediate posttreatment effect of thoracic and rib thrust techniques with regard to pain and shoulder ROM in patients with subacromial impingement157,158 but also mediumand long-term (up to 1 year) benefits of thrust and nonthrust interventions to the cervicothoracic spine, ribs, shoulder, and shoulder girdle over or in addition to exercise, medical care, and steroid infiltration.159,160 Recent systematic reviews including a Cochrane Review161,162 have supported a combination of manual therapy and exercise for patients with impingement for improvements in pain and function. A systematic review of RCTs on patients with painful shoulder conditions noted significant increases in ROM favoring manual therapy including Mulligan MWM techniques, Maitland midrange oscillations, and Kaltenborn glide mobilizations to the glenohumeral joint, a trend for manual therapy in reducing pain, but inconclusive evidence for effects on quality of life or function.163 A case series and an RCT have shown significant effects of nonthrust glenohumeral techniques on ROM and disability maintained for 9 to 12 months in patients with adhesive capsulitis with end-range mobilizations seemingly more effective than midrange techniques.164,165

Elbow Dysfunction A cohort study with a heterogeneous group of patients with upper extremity overuse syndromes including lateral epicondylalgia of the elbow reported significant changes with regard to pain and function after 4 weeks of ART intervention.42 In a case report, Howitt166 reported on the successful rehabilitation of a patient with chronic lateral epicondylalgia using Graston and ART combined with exercise and modalities. Haller and associates167 reported on the successful use of ASTYM in a patient with chronic lateral epicondylalgia. A Cochrane Review168 noted no consistent benefit of deep friction massage over other physical therapy approaches with regard to pain or grip strength in patients with epicondylalgia but a more recent RCT showed significant between-group differences favoring deep friction massage and Mill’s manipulation of the elbow over diclofenac, phonophoresis, and supervised exercise with regard to (pain-free) grip strength and function at 4 weeks.169 A systematic review noted insufficient evidence for long-term effects of manual therapy but evidence for positive immediate effects of elbow manipulation.170 A more recent RCT comparing MWM techniques to the elbow combined with exercise to corticosteroid infiltration and “wait-and-see” showed that the manual

48

588  Physical Modalities for Pain Management

therapy intervention was superior to wait-and-see at 6 weeks and superior to the infiltration after 6 weeks with high recurrence rates in the latter group.171 In an RCT Struijs and colleagues172 compared palmar scaphoid gliding manipulation and passive wrist ROM with a control treatment of friction massage, ultrasound, and strengthening for lateral epicondylalgia and reported a significant betweengroup difference on a global measure of improvement at 3 weeks and on pain at 6 weeks—both favoring the manipulation group. Earlier we discussed the preliminary development of a treatmentbased classification for patients with lateral epicondylalgia.111

Wrist and Hand Dysfunction Burke and coworkers173 found no significant between-group differences when comparing Graston technique with manual soft tissue techniques in patients with carpal tunnel syndrome (CTS) at 6 weeks but significant within-group effects for both groups on electrodiagnostic findings, wrist strength, and wrist ROM, which were maintained at 3 months. In a case report, Baker and Wilson174 reported on successful management of a patient with chronic bilateral carpal tunnel syndrome using the ASTYM method. In patients with CTS scheduled for surgery, Tal-Akabi and Rushton175 compared neurodynamic mobilization or carpal gliding mobilization and flexor retinaculum stretching to a control group. They reported significant within-group improvements with regard to pain and ROM for both mobilization groups and significant between-group differences favoring both experimental groups over the control group with regard to pain. Six of seven subjects in the control group proceeded with surgery, whereas 11 of 14 in the mobilization groups cancelled surgery. Two systematic reviews176,177 have since recommended carpal bone mobilization for the management of patients with CTS. The efficacy of manual therapy for patients after distal radius fracture with regard to ROM and pain is less clear: A systematic review noted that manual mobilization for Colles fracture was not supported by an RCT but did show positive outcomes in a case series design.178 Nonthrust traction and gliding mobilization of the metacarpophalangeal (MCP) joints after metacarpal fracture has shown significant effects with regard to ROM and joint stiffness over a home exercise program in an RCT.179 Two case reports have described the use of MWM techniques after MCP I dysfunction.29,180 Also in a case report, Howitt and associates181 described the use of Graston and ART in a patient with flexor pollicis longus tenosynovitis.

Hip Dysfunction colleagues182

In an RCT Hoeksma and showed significant effects on perceived improvement, pain, stiffness, hip function, and ROM persisting at 29 weeks after 5 weeks of muscle stretching, nonthrust hip mobilization, and thrust traction manipulation to the hip joint over specific exercise instruction in patients with osteoarthritis of the hip. Similar results were found in a case series replicating this intervention.183 The outcome of this manual therapy intervention was better in patients with mild or moderate versus severe osteoarthritis.184

Knee Dysfunction A Cochrane Review168 noted no benefit for friction massage over other physical therapy management for patients with iliotibial band friction syndrome at the knee. Henry and colleagues185

reported on the positive outcomes use of ASTYM in a patient with bilateral total knee arthroplasty. Also in a case report, Henry and associates186 described the successful treatment of a patient postpatellar fracture with ASTYM after 3 months of failed conventional therapy. A cohort study in patients with anterior knee pain showed no immediate postintervention effect of ART on muscle inhibition and strength of the quadriceps muscle.187 In an RCT, Wilson and colleagues188 showed superior outcomes on patientreported pain and function for treatment of patellar tendinopathy using ASTYM and a home program over a similar home program and stretching, deep friction massage, and modalities at therapist discretion. An RCT showed significant between-group differences with regard to walking distance and various WOMAC scores at 4  weeks in patients with knee osteoarthritis favoring manual therapy techniques to the lumbar and lower extremity joints combined with a home program over subclinical ultrasound. In the experimental group, these improvements over baseline were maintained at 1 year and only 5% of the experimental group versus 20% of the control group proceeded to have knee arthroplasty surgery.189 Also in an RCT, Pollard and coworkers190 reported significant between-group differences for treatment with soft tissue and thrust techniques to the tibiofemoral and patellofemoral joints over sham manipulation with regard to knee pain and self-report of crepitus, mobility, and function at 6 weeks in patients with osteoarthritic knee pain.

Ankle and Foot Dysfunction In a case report, Hammer156 reported on the use of Graston technique in the management of patients with plantar fasciitis and Achilles tendinosis. Also in a case report, Howitt and associates191 described the use of Graston and ART in a patient with posterior tibial strain. Melham and colleagues192 reported in a case report on the effective use of ASTYM in a patient with a chronic painful fibrotic ankle. A systematic review reported an initial positive effect on dorsiflexion ROM for the use of Mulligan MWM, Kaltenborn glide mobilization, and manipulation of the ankle mortise in patients after ankle sprain.193 In contrast, adding talar glide mobilization to other physical therapy management did not result in significant between-group differences with regard to function or quality of life in an RCT with patients after isolated ankle fracture.194

Systemic Conditions Holey49 noted that there was no evidence for the use of connective tissue massage in patients with subacute asthma but that it has been shown to reduce menopausal symptoms. Brantberg and colleagues195 reported significant differences in pain and quality of life favoring connective tissue massage over group counseling in patients with fibromyalgia.

Lymphedema A systematic review noted that there was some evidence to suggest that compressive therapy and manual lymphatic drainage might improve lymphedema related to breast cancer surgery.196 A systematic review including randomized, cohort, pilot, and case studies indicated that manual lymphatic drainage resulted in significant positive effects on pain, edema, and ROM after ankle sprains and on edema in wrist fractures.197

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Contraindications and Evidence on Risk of Harm

Table 48-5  Contraindications and Precautions for Manipulation Contraindications

Bone

Contraindications Even in massage therapy textbooks, contraindications and precautions for massage vary greatly and generally are not based on research evidence.198 However, common sense can serve as a guide. Vigorous massage would seem contraindicated in patients with bleeding disorders, low platelet counts, and those on anticoagulant medication. Massage should not be done in areas where there are skin infections, abscesses, open wounds, fractures, weakened bones, or blood clots (including deep venous thrombosis, severe varicose veins, and thrombophlebitis). Recent surgical scars serve as a precaution. There is no evidence of adverse effects of massage in patients with cancer but direct deep pressure over a tumor would seem unwise and patients should likely consult their oncologist prior to massage treatments.50,199 Although often noted as a contraindication, Bauer and associates200 showed no deleterious effect of massage on heart rate and blood pressure even in patients as early as 48 to 72 hours postmyocardial infraction. Gibbons & Tehan56 emphasized appropriate patient selection and appropriate technique as perhaps the most important method for preventing—or at least limiting—adverse events with manipulation. They also provided a list of precautions and contraindications to manipulation that also equally apply to nonthrust techniques and other manual therapy interventions (Table 48-5).

Evidence on Risk of Harm Associated with Massage Perhaps more relevant to the risk-benefit analysis involved in clinical decision-making than the contraindications and precautions just mentioned is research evidence on risk of harm. In a systematic review, Ernst48 reported adverse events, including a cerebrovascular accident, displacement of a urethral stent, kidney embolization, hepatic and musculoskeletal hematoma, leg ulcers, nerve damage including posterior interosseus syndrome, pseudoaneurysm, pulmonary embolism, thyrotoxicosis in a patient with Hashimoto syndrome, and various pain syndromes. Another systematic review201 added to these myositis ossificans in a patient treated for a thigh contusion, unilateral sensorineural hearing loss after trapezius massage, and perforation of the sigmoid colon. Ernst48 noted that serious adverse events were associated mostly with massage techniques other than Swedish massage and generally involved unlicensed practitioners and only very rarely licensed massage therapists. Based on his systematic review, Grant201 cautioned against treatment in patients using anticoagulant medication or with implanted medical devices and suggested caution with work near superficial nerves and the use of manual lymphatic drainage only over contusions.

Minor Adverse Events Associated with Manipulation For decision-making with regard to manual therapy interventions, clinicians should again combine the previously mentioned common sense precautions and contraindications with research evidence on risk of harm. Manual therapy frequently results in minor adverse events that are of short duration and the ill effects of which

Neurologic

Any pathology that may lead to significant bone weakening ll Tumor (primary or metastatic) ll Infection (e.g., tuberculosis) ll Metabolic (e.g., osteomalacia) ll Congenital dysplasia ll Iatrogenic including long-term corticosteroid use ll Inflammatory (e.g., severe rheumatoid arthritis) ll Trauma or fracture ll ll ll ll

Vascular

ll

ll ll

Cervical myelopathy Spinal cord compression Cauda equina syndrome Radicular compression with progressive neurologic deficit Diagnosed cervical artery dysfunction Aortic aneurysm Bleeding diatheses (­hemophilia)

Lack of a diagnosis Lack of patient consent Patient positioning inadequate Precautions

ll

ll ll ll ll ll ll ll ll ll

ll

Unable to properly position patient for technique due to pain or resistance

Adverse reactions to previous manual therapy interventions Disk herniation Inflammatory arthritides Pregnancy Spondylolysis/spondylolisthesis Osteoporosis Anticoagulant or long-term corticosteroid use Advanced degenerative joint disease/spondylosis Vertigo Psychological dependence on manual therapy intervention Atherosclerosis

Modified from Gibbons and Tehan 2001.

fully resolve. A retrospective survey of Maitland-trained physical therapists reported on 228,050 thrust techniques compared to nonthrust spinal techniques.202 Of all patients treated with manipulation, 29 noted 52 adverse events. Four of these occurred with lumbar and thoracic manipulation and included sciatic pain, an increase in LBP, and—admittedly less minor—two rib fractures. Cervical thrust techniques resulted in 12 patients complaining of postmanipulation dizziness, 11 of nausea, 10 of severe headache, 3 each of nystagmus, blurred vision, vomiting, and brachialgia, and 1 each of brachialgia with neurologic deficit, loss of consciousness, and acute wry neck. Average recovery time was 6.3 days and there were no lasting sequelae. Of patients treated with mobilization techniques, 58 had 129 complications: 39 complained of dizziness, 35 of severe headache, 28 of nausea, 6 of brachialgia with

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neurologic deficit, 4 of simple brachialgia, 5 of blurred vision, 4 of vomiting, 3 of nystagmus or increased pain lasting more than 2 weeks, and one of immediate postintervention skin clamminess. Somewhat counter to assumptions about comparative safety, one cervical mobilization (not manipulation) session was temporally associated with a cerebrovascular accident (CVA) with limited but prolonged neurologic deficits. Michaeli202 calculated an incidence of one adverse event per 3020 cervical manipulations, whereas he noted only one adverse event per 38,137 lumbothoracic manipulations. In a prospective study on 283 patients seeing physiotherapists, osteopaths, and chiropractors for manipulative interventions, 60.9% of patients reported at least one postmanipulative reaction. Most common were headache (19.8%), stiffness (19.5%), local discomfort (15.2%), radiating discomfort (12.1%), and fatigue (12.1%). Less common were muscle spasm (5.84%), dizziness (4.28%), and nausea (2.72%). Most of these reactions began within 4 hours and generally disappeared within the next 24 hours. Upper cervical manipulation (OR 3.20, 95% CI 1.89 to 7.77), use of medication (OR 2.20, 95% CI 1.31 to 3.69), female gender (OR 1.66, 95% CI 1.01 to 2.75), and increasing age (OR 1.02, 95% CI 1.00 to 1.05) were found to be independent predictors of headache after spinal manipulation.203 In an RCT studying patients with mechanical neck pain and comparing chiropractic upper thoracic and/or cervical mobilization to manipulation, both with or without modalities, 280 of 336 (83%) subjects responded to a questionnaire sent 2 weeks after treatment. Of these 280, 85 subjects reported 212 adverse reactions: 48 patients treated with manipulation noted 120 symptoms, whereas 37 patients with mobilization noted 92 symptoms. Increased neck pain or stiffness was most common (25%). Headache, tiredness or fatigue, and radiating pain or discomfort were reported by 15.7%, 10%, and 6.1% of subjects, respectively. Less common but still reported by at least 1% of subjects were dizziness or imbalance, extremity weakness, ringing in the ears, depression or anxiety, nausea or vomiting, blurred or impaired vision, and confusion or disorientation. The majority of symptoms started within 24 hours of the manual therapy treatment, disappeared within 24 hours of onset, and did not greatly impair normal activities. Subjects receiving manipulation were more likely than those receiving mobilization to report an adverse reaction (OR 1.44, 95% CI 0.85 to 2.43). Manipulation subjects also were more likely to have symptoms commencing within 24 hours of treatment and with higher severity levels (OR 1.44, 95% CI 0.83 to 2.49). Subjects with moderate to severe headaches were more likely than those with only mild to no headaches to report headache as an adverse treatment reaction (OR 5.18, 95% CI 1.88 to 14.3). Patients with Neck Disability Index scores indicative of moderate to severe neck disability were more likely than those with less neck disability to report dizziness, nausea, blurred or impaired vision, ringing in the ears, extremity weakness, and confusion (OR 3.15, 95% CI 1.01 to 9.80) possibly indicative of more serious neurovascular pathology.204 Minor adverse events after manual therapy seem very common. It should be noted that fatigue, drowsiness, headache, dizziness, nausea, and difficulty concentrating are among the most common nonspecific drug-related adverse effects and that these symptoms are frequently reported even by subjects in the placebo arm of drug trials. In general population studies, up to 75% report these symptoms in preceding 3 days.204 Still, clinicians can use these data to educate patients on the possible occurrence of

these short-lived side-effects. With the Michaeli202 survey constituting a lower level of evidence than the Hurwitz and colleagues RCT,204 it would seem that, especially in the cervical spine, thrust techniques produce more adverse reactions than nonthrust techniques, although the nonthrust techniques are certainly implicated in producing minor and also major adverse events. The predictor variables derived from the above studies can help in patient and technique selection. Hurwitz and coworkers204 suggested that clinicians should be cautious about using cervical spine manipulation, especially in those patients with more severe neck-related disability.

Major Adverse Events Associated with Manipulation Of course, major adverse events characterized by prolonged and only partially reversible or irreversible sequelae can also occur after spinal manipulation. Systematic reviews205-209 have reported clinically worsened disc herniation or cauda equina syndrome with lumbar manipulation and rib fractures with thoracic manipulation. Dissection of the vertebral and carotid arteries, dural tears, nerve injury including phrenic nerve palsy, cervical disc herniation, epidural or flaval ligament hematoma, spinal cord injuries (myelopathy, quadriparesis, central cord syndrome or paraparesis), and fractures involving a spondylotic cervical fusion, a cervical transverse process, the C2, C5, and C6 vertebral bodies, and the odontoid process have all been associated with cervical manipulation. Van Tulder and associates208 indicated that the risk of serious adverse events with lumbar spine manipulation is limited when the intervention is used by a trained clinician. Earlier we discussed limited evidence for the therapeutic effect of manipulation on disc herniation and we noted disc herniation as a precaution, although not a contraindication to manual therapy interventions. The major adverse event associated with lumbar manipulation is progression of a disc herniation perhaps even leading to progression of neurologic compromise including radiculopathy and cauda equina syndrome. Based on a systematic review of the literature, Oliphant59 calculated a highest risk estimate for developing a disc herniation or cauda equina attributable to treatment of lumbar disc herniation by spinal manipulation as one in 3.72 million manipulations. Despite this low-risk estimate, careful patient selection and consideration of other management options are strongly indicated. Evidence linking cervical manipulation to cervical (vertebral and internal carotid) artery dysfunction (CAD) and subsequent CVA has included multiple narrative reviews of case reports found in the literature.210-213 Hurwitz and colleagues214 acknowledged the likely high underreporting bias and noted an estimated risk adjusted for an only 10% reporting rate in the literature of 5 to 10 per 10 million for all complications, 6 in 10 million for serious complications, and 3 in 10 million for the risk of death. Haneline and coworkers215 found 13 cases of internal carotid artery dissection temporally associated with cervical manipulation in a 1966 to 2000 Medline review and estimated the chance of developing CAD in this artery postmanipulation at 1 in 601,145,000. The possible cause-and-effect relationship between cervical manipulation and CAD remains a contentious issue.216 Research into risk of harm is wrought with methodologic shortcomings and not only because of the obvious ethical concerns with studies that would prospectively expose patients to a suspected risk factor.217 In the context of risk of harm, it would seem prudent to consider the epidemiologic Bradford-Hill criteria that state a cause-and-effect

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relationship becomes likely when the following criteria are all met:213 1. The proposed relationship is biologically plausible. 2. The proposed cause is temporally related to the occurrence. 3. The relationship is consistent across different samples and groups. 4. There exists a positive correlation between exposure and occurrence. 5. There exists no other plausible explanation. Although opinions certainly and justifiably differ, case reports and narrative reviews provided by authors in diverse geographic locations temporally linking possible mechanical trauma of the cervical arteries owing to manipulation to CAD would seem to qualify as supporting the first three criteria. Exploring the criterion of a correlation between exposure to manipulation and occurrence of CAD, Rothwell and associates218 compared 582 patients with vertebrobasilar accidents over the period 1993 to 1998 with age and sexmatched controls from the provincial insurance database in Ontario, Canada. They also determined exposure to ­chiropractic using this same database. These authors found that subjects younger than 45 years were five times more likely (95% CI 1.31 to 43.87) to have visited a chiropractor in the month preceding the stroke. This same age group was also five times (95% CI 1.34 to 18.57) more likely to have had three or more visits with cervical or thoracic spinerelated complaints or headache in the month prior to the stroke. No significant association was noted for subjects older than 45 years.

However, Cassidy and colleagues219 used a very similar study design comparing 818 patients with vertebrobasilar accidents to age- and sex-matched controls from a provincial insurance database and also found an OR of 3.13 (95% CI 0.52 to 1.32) for having visited a chiropractor in the month before the stroke in those younger than 45 years, whereas the OR was 0.83 (95% CI 0.52 to 1.32) for those older than 45 years. In addition, these researchers looked at visits to general medical practitioners preceding the stroke and found an OR of 3.57 (95% CI 2.17 to 5.86) for those under 45 years and 2.67 (95% CI 2.25 to 3.17) for patients having visited their medical doctor in the month preceding the vertebrobasilar accident. Cassidy and coworkers219 suggested that the similar association between chiropractic and medical visits might indicate that patients with an undiagnosed dissection seek clinical care for headache and neck pain before having a CVA versus lending credence to an exposureand-occurrence relationship between manipulation and CAD. With regard to the criterion of other plausible explanations, CAD can occur associated with major trauma but more relevant in this context is spontaneous CAD defined as dissection associated with minor trauma, including but not limited to, sporting activities, whiplash injury, stretches, sudden neck movements, severe coughing, all in addition to cervical manipulation.220 Even without a conclusive answer with regard to a causal relationship between manipulation and CAD, it would certainly seem prudent for clinicians to be vigilant for patients presenting with signs and symptoms of a cervical artery dissection in progress. Table 48-6 provides

Table 48-6  Nonischemic and Ischemic Signs and Symptoms of Cervical Artery Dysfunction Vertebral and Basilar Arteries

Internal Carotid Artery

Nonischemic

Ipsilateral posterior neck pain Ipsilateral occipital headache Sudden onset and severe Described as stabbing, pulsating, aching, “thunderclap,” sharp, or of an unusual character: “ a headache unlike any experienced before” Very rarely radicular symptoms C5-6 (due to local neural ischemia)

Ipsilateral upper and midcervical spine pain Ipsilateral frontal-temporal or periorbital headache Sudden onset, severe, and of an uncommon character Horner syndrome Pulsatile tinnitus Cranial nerve palsies Ipsilateral carotid bruit Neck swelling Scalp tenderness Anhidrosis of face

Ischemic

Dizziness Drop attacks Diplopia (including amaurosis fugax and corneal reflux) Dysarthria Dysphagia (including hoarseness and hiccups) Ataxia of gait Nausea Numbness (in ipsilateral face and/or contralateral body) Nystagmus Vomiting Loss of short-term memory Vagueness Hypotonia and limb weakness affecting arm or leg Anhidrosis: lack of facial sweating Hearing disturbances Malaise Perioral dysesthesia Photophobia Clumsiness Agitation Cranial nerve palsies Hindbrain stroke: Wallenberg or locked-in syndrome

Transient ischemic attack Middle cerebral artery distribution stroke Retinal infarction Amaurosis fugax: temporary blindness Localized patchy blurring of vision: scintillating scotomata Weakness extraocular muscles Protrusion of the eye Swelling of the eye or conjunctiva

48

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diagnostic information on nonischemic presentations of internal carotid and vertebral artery dysfunction.221,222

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155. van den Dolder PA, Roberts DL. A trial into the effectiveness of soft tissue massage in the treatment of shoulder pain. Aust J Physiother. 2003;49:183. 156. Hammer WI. The effect of mechanical load on degenerated soft tissue. J Bodyw Mov Ther. 2008;12:246. 157. Boyles RE, Ritland BM, Miracle BM, et al. The short-term effects of thoracic spine thrust manipulation on patients with shoulder impingement syndrome. Man Ther. 2009;14:375. 158. Strunce JB, Walker MJ, Boyles RE, Young BA. The immediate effects of thoracic spine and rib manipulation on subjects with primary complaints of shoulder pain. J Man Manip Ther. 2009;17:230. 159. Bang MD, Deyle GD. 2000 Comparison of supervised exercise with and without manual physical therapy for patients with shoulder impingement syndrome. J Orthop Sports Phys Ther. 2000;30:126. 160. Bergman GJD, Winters JC, Groenier KH, et al. Manipulative therapy in addition to usual medical care for patients with shoulder dysfunction and pain: a randomized, controlled trial. Ann Intern Med. 2004;141:432. 161. Faber E, Kuiper JI, Burdorf A, et al. Treatment of impingement syndrome: a systematic review of the effects on functional limitations and return to work. J Occup Rehabil. 2006;16:7. 162. Green S, Buchbinder R, Hetrick SE. Physiotherapy interventions for shoulder pain. Cochrane Database Syst Rev. 2003:Issue 2 Art No CD004258. 163. Camarinos J, Marinko L. Effectiveness of manual physical therapy for painful shoulder conditions: a systematic review. J Man Manip Ther. 2009;17:206. 164. Vermeulen HM, Obermann WR, Burger BJ, et al. End-range mobilization techniques in the treatment of adhesive capsulitis of the shoulder joint: A multiple-subject case report. Phys Ther. 2000;80:1204. 165. Vermeulen HM, Rozing PM, Obermann WR, et al. Comparison of high-grade and low-grade mobilization techniques in the management of adhesive capsulitis of the shoulder: randomized clinical trial. Phys Ther. 2006;86:355. 166. Howitt SD. Lateral epicondylosis: a case study of conservative care using ART and rehabilitation. J Can Chiropr Assoc. 2006;50:182. 167. Haller KH, Helfst RH, Wilson JK, Sevier TL. Treatment of chronic elbow pain. Phys Ther Case Rep. 1999;2(5):195. 168. Brosseau L, Casimiro L, Milne S, et al. Deep transverse friction massage for treating tendonitis. Cochrane Database Syst Rev. 2002;4. 169. Nagrale AV, Herd C, Ganvir S, Ramteke G. Cyriax physiotherapy versus phonophoresis with supervised exercise in subjects with lateral epicondylalgia: a randomized clinical trial. J Man Manip Ther. 2009;17:171. 170. Bisset L, Paungmali A, Vicenzino B, Beller E. A systematic review and meta-analysis of clinical trials on physical interventions for lateral epicondylalgia. Br J Sports Med. 2005;39:411. 171. Bisset L, Beller E, Jull G, et al. Mobilisation with movement, corticosteroid injection, or wit and see for tennis elbow: randomised trial. BMJ. 2006;333:939. 172. Struijs PA, Damen PJ, Baller EW, et al. Manipulation of the wrist for management of lateral epicondylitis: a randomized pilot study. Phys Ther. 2003;83:608. 173. Burke J, Buchberger DJ, Carey-Loghmani MT, et al. A pilot study comparing two manual therapy interventions for carpal tunnel syndrome. J Manipulative Physiol Ther. 2007;30:50. 174. Baker D, Wilson JK. Bilateral carpal tunnel syndrome in a piano teacher. Phys Ther Case Rep. 1999;2(2):73. 175. Tal-Akabi A, Rushton A. An investigation to compare the effectiveness of carpal bone mobilisation and neurodynamic mobilisation as methods of treatment for carpal tunnel syndrome. Man Ther. 2000;5:214. 176. Muller M, Tsui D, Schnurr R, et al. Effectiveness of hand therapy interventions in the primary management of carpal tunnel syndrome: a systematic review. J Hand Ther. 2004;17:210. 177. O’Connor D, Marshall SC, Massy-Westropp N. Non-surgical treatment (other than steroid injection) for carpal tunnel syndrome. Cochrane Database Syst Rev. 2003:Issue 1. Art. No.: CD003219.

48

596  Physical Modalities for Pain Management 178. Michlovitz SL, Harris BA, Watkins M. Therapy interventions for improving joint range of motion: A systematic review. J Hand Ther. 2004;17:118. 179. Randall T, Portney L, Harris BA. Effects of joint mobilization on joint stiffness and active motion of the metacarpal-phalangeal joint. J Orthop Sports Phys Ther. 1992;16:30. 180. Folk B. Traumatic thumb injury management using mobilization with movement. Man Ther. 2001;6:178. 181. Howitt S, Wong J, Zabukovec S. The conservative treatment of trigger thumb using Graston Techniques and Active Release Techniques. J Can Chiropr Assoc. 2006;50:249. 182. Hoeksma HL, Dekker J, Ronday HK, et al. Comparison of manual therapy and exercise therapy in osteoarthritis of the hip: a randomized clinical trial. Arthritis Rheum. 2004;51:722. 183. MacDonald CW, Whitman JM, Cleland JA, et al. Clinical outcomes following manual physical therapy and exercise for hip osteoarthritis: A case series. J Orthop Sports Phys Ther. 2006;36:588. 184. Hoeksma HL, Dekker J, Ronday HK, et al. Manual therapy in osteoarthritis of the hip: outcome in subgroups of patients. Rheumatology. 2005;44:461. 185. Henry P, Panwitz B, Wilson JK. Treatment of a bilateral total knee replacement using augmented soft tissue mobilization. Phys Ther Case Rep. 1999;2(1):27. 186. Henry P, Panwitz B, Wilson JK. Rehabilitation of a post-surgical patella fracture: A case study. Physiother. 2000;86(3):139. 187. Drover JM, Forand DR, Herzog W. Influence of active release technique on quadriceps inhibition and strength: a pilot study. J Manipulative Physiol Ther. 2004;27:408. 188. Wilson JK, Sevier TL, Helfst RH, et al. Comparison of rehabilitation methods in the treatment of patellar tendinitis. J Sport Rehabil. 2000;9:304. 189. Deyle GD, Henderson NE, Matekel RL, et al. Effectiveness of manual physical therapy and exercise in osteoarthritis of the knee. A randomized, controlled trial. Ann Intern Med. 2000;132:173. 190. Pollard H, Ward G, Hoskins W, Hardy K. The effect of a manual therapy knee protocol on osteoarthritic knee pain: a randomised controlled trial. J Can Chiropr Assoc. 2008;52:229. 191. Howitt S, Jung S, Hammonds N. Conservative treatment of a tibialis posterior strain in a novice triathlete: a case report. J Can Chiropr Assoc. 2009;53:23. 192. Melham TJ, Sevier TL, Malnofski MJ, et al. Chronic ankle pain and fibrosis successfully treated with a new noninvasive augmented soft tissue mobilization technique (ASTM): a case report. Med Sci Sports Exerc. 1998;30:801. 193. van der Wees PJ, Lenssen AF, Hendriks EJ, et al. Effectiveness of exercise therapy and manual mobilisation in acute ankle sprain and functional instability: a systematic review. Aust J Physiother. 2006;52:27. 194. Lin CW, Moseley AM, Haas M, et al. Manual therapy in addition to physiotherapy does not improve clinical or economic outcomes after ankle fracture. J Rehabil Med. 2008;40:433. 195. Brattberg G. Connective tissue massage in the treatment of fibromyalgia. Eur J Pain. 1999;3:235. 196. Kligman L, Wong RK, Johnston M, Laetsch NS. The treatment of lymphedema related to breast cancer: a systematic review and evidence summary. Support Care Cancer. 2004;12:421. 197. Vairo GL, Miller SJ, McBrier NM, Buckley WE. Systematic review of efficacy of manual lymphatic drainage techniques in sports medicine and rehabilitation: an evidence-based practice approach. J Man Manip Ther. 2009;17:E80. 198. Batavia M. Contraindications for therapeutic massage: Do sources agree? J Bodyw Mov Ther. 2004;8:48. 199. Vickers A, Zollman C. ABC of complementary medicine. Massage therapies. BMJ. 1999;319:1254. 200. Bauer WC, Dracup KA. Physiological effects of back massage in patients with acute myocardial infarction. Focus on Critical Care. 1987;14(6):42.

201. Grant KE. Massage safety: Injuries reported in Medline relating to the practice of therapeutic massage 1965-2003. J Bodyw Mov Ther. 2003;7:207. 202. Michaeli A. Reported occurrence and nature of complications following manipulative physiotherapy in South Africa. Aust J Physiother. 1993;39:309. 203. Cagnie B, Vinck E, Beernaert A, Cambier D. How are side effects of spinal manipulation and can these side effects be predicted? Man Ther. 2004;9:151. 204. Hurwitz EL, Morgenstern H, Vassilaki M, Chiang LM. Frequency and clinical predictors of adverse reactions to chiropractic care in the UCLA neck pain study. Spine. 2005;30:1477. 205. Assendelft WJ, Bouter LM, Knipschild PG. Complications of spinal manipulation: a comprehensive review of the literature. J Fam Pract. 1996;42(5):475. 206. Ernst E. Adverse effects of spinal manipulation: a systematic review. J R Soc Med. 2007;100:330. 207. Kraft CN, Conrad R, Vahlensieck M, et al. Nicht-zerebrovaskuläre Komplikationen der chirotherapeutischen HWS-Manipulation. Z Orthop. 2000;138:8. 208. van Tulder MW, Koes B, Malmivaara A. Outcome of non-­invasive treatment modalities on back pain: an evidence-based review. Eur Spine J. 2006;15:S64. 209. Cherkin DC, Sherman KJ, Deyo RA, Shekelle PG. A review of the evidence for the effectiveness, safety, and cost of acupuncture, massage, and spinal manipulation for back pain. Ann Intern Med. 2003;138:898. 210. DiFabio RP. Manipulation of the cervical spine: risks and benefits. Phys Ther. 1999;79:50. 211. Ernst E. Manipulation of the cervical spine: a systematic review of case reports of serious adverse events, 1995-2001. Med J Aust. 2002;176:376. 212. Terrett AGJ. Vertebrobasilar stroke following spinal manipulation therapy. In: Murphy DR, ed. Conservative Management of Cervical Spine Syndromes. New York: McGraw-Hill; 2000:553-578. 213. Triano JJ, Kawchuk G. Current Concepts: Spinal Manipulation and Cervical Arterial Incidents. Clive, Iowa: NCMIC; 2006. 214. Hurwitz EL, Aker PD, Adams AH, et al. Manipulation and mobilization of the cervical spine. A systematic review of the literature. Spine. 1996;21:1746. 215. Haneline MT, Croft AC, Frishberg BM. Association of internal carotid artery dissection and chiropractic manipulation. Neurologist. 2003;9:35. 216. Huijbregts PA, Oostendorp RAB. Cervical artery dissection and manipulation: a review of relevant research with implications for diagnosis and management. Interdiv Rev Jan/Feb:23. 2010. 217. Rubinstein SM, Peerdeman SM, van Tulder MW, et al. A systematic review of the risk factors for cervical artery dissection. Stroke. 2005;36:1575. 218. Rothwell DM, Bondy SJ, Williams JI. Chiropractic manipulation and stroke: a population-based case control study. Stroke. 2001;32:1054. 219. Cassidy JD, Boyle E, Cote P, et al. Risk of vertebrobasilar stroke and chiropractic care: results of a population-based case-control and casecrossover study. Spine. 2008;33:S176. 220. Debette S, Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurol. 2009;8:668. 221. Kerry R, Taylor AJ. Cervical arterial dysfunction assessment and manual therapy. Man Ther. 2006;11:243. 222. Kerry R, Taylor AJ, Mitchell J, et al. Manual therapy and cervical arterial dysfunction, directions for the future: a clinical perspective. J Man Manip Ther. 2008;16:39. 223. Childs JD, Whitman JM, Sizer PS, et al. A description of physical therapists’ knowledge in managing musculoskeletal conditions. BMC Musculoskelet Disord. 2005;6:32.

Therapeutic Exercises

49

Joel D. Sebag, DPT

Therapeutic exercises or exercise therapy is a major component in the management of various disorders. It can be defined as any prescribed and supervised exercise program, in which, during therapy sessions, the patients are required to carry out repeated voluntary dynamic movements or static muscle contractions, either whole body or region specific and either with or without external loading with the aim of relieving symptoms or improving function, by controlling inflammation, when present, restoring range of motion (ROM), restoring and/or improving muscular strength, power and endurance, and training to return to daily and recreational activities.1-4 The prescription and application of patient-specific therapeutic exercises for patients with musculoskeletal pain conditions can be a confusing and challenging endeavor even for the experienced clinician because of the great variety in content, technique, and method of delivery. Typically, the choice of exercise program would be influenced by the therapists’ own training and experience. The purpose of this chapter is to help readers make informed choices based on available research evidence as well as clinical training and experience. The chapter will discuss the type and intensity of exercises to be used for the management of conditions associated with neck, shoulder, back, hip, and knee pain, with detailed description and guidance on various therapeutic exercises as well as discussions of the research evidence available on the efficacy of therapeutic exercises for these conditions. The available research evidence is based largely on systematic reviews, such as Cochrane reviews, where they were available, and also is taken from the recommendations of the Philadelphia Panel Evidence-Based Clinical Guidelines on Rehabilitation Interventions. Convened in 1999, the Philadelphia Panel, composed of clinical experts in the fields of medicine, research, and physical therapy set out to provide a structured and rigorous set of evidence-based guidelines for the conservative (nonsurgical) management of conditions associated with low back, knee, neck, or shoulder pain. A five-step process was established to put together these guidelines: defining rehabilitation interventions most frequently used in the care of low back, knee, neck, and shoulder pain, collecting the evidence, synthesizing the results, making recommendations based on the research, and grading the strength of the recommendations.5 The panel gathered evidence from randomized clinical trials and observational studies; the data were synthesized, and the relative clinical benefit between treatment and control groups was calculated for each condition for each intervention. The studies were also graded according to type and clinical importance of the findings. The grading scheme is summarized in Table 49-1. The

panel deemed a 15% or greater improvement between treatment and control groups to be clinically important. In addition, the panel circulated feedback survey questionnaires to healthcare practitioners to verify their applicability and ease of use in clinical settings. Interventions with a grade of A or B were to be included in the guidelines.5 Briefly, the panel gave Grade A recommendation on the efficacy of therapeutic exercises, including stretching, strengthening, and mobility exercises for the treatment of subacute, chronic, postsurgery back pain, osteoarthritis of the knee, and chronic neck pain. Grade A recommendation means the intervention resulted in clinically significant improvement in pain and function. However, there are insufficient data on the benefit of therapeutic exercises for shoulder pain.5 These recommendations were made based on the available evidence at the time. The Philadelphia Panel also noted in its recommendation, many problems with the body of evidence in the medical literature—the main concern being the lack of standardization of outcome measurements used in different studies. Also noted was the inherent difficulty of studying rehabilitation interventions, where effectiveness could be compromised by psychosocial, physical, and occupational factors, as well as improbability of blinding either the therapist or the patient to the interventions.5 To address these issues, the panel recommends that future studies develop standards of measurement that are valid, reliable, and sensitive to changes in outcome; further, studies must specifically clarify the type and manner of intervention, intervention intensity and duration, and progression of the intervention according to patient-specific outcomes. Studies need to fully randomize large patient groups to minimize selection bias. Overall, the panel stressed the need for further large studies on rehabilitation interventions with the increased use of therapeutic exercises and other physical therapy interventions for the management of low back pain, knee pain, neck pain, and shoulder pain.5 Smidt and colleagues1 summarized and assessed available evidence on the effectiveness of exercise therapy for patients with disorders of the musculoskeletal and other systems. In their assessment of 98 reviews, they concluded that exercise therapy is effective for a wide range of chronic disorders. In particular, they found exercise therapy is effective for patients with knee osteoarthritis, subacute and chronic low back pain, cystic fibrosis, chronic obstructive pulmonary disease (COPD), and intermittent claudication. They also found indications that exercise therapy is effective for patients with ankylosing spondylitis, hip osteoarthritis, and Parkinson disease, and also for patients who have had stroke. They could not find 597

598  Physical Modalities for Pain Management

sufficient evidence to support or refute effectiveness of therapeutic exercises for patients with neck pain, shoulder pain, repetition strain injury (RSI), rheumatoid arthritis, asthma, and bronchiectasis. However, there is insufficient evidence to support or refute the effectiveness of specific types of therapeutic exercises for all disorders, and there is little or no research on how short-term effectiveness of the exercise therapies can be maintained long term. Conversely, they found no evidence that exercise therapy is harmful or that it provoked harmful side effects. They suggested that is could be due to the inadequate reporting of side effects in ­randomized controlled trials.1

Table 49-1  Details of the Philadelphia Panel Classification System Grade

Clinical Importance

Study design type

A

15%

RCT (single or meta-analysis)

B

15%

CCT or observational study (single  or meta-analysis)

C

15%

RCT or CCT or observational (single  or meta-analysis)

ID

NA

Insufficient or no data

CCT, controlled clinical trial; NA, not applicable; RCT, randomized, controlled trial From Harris GR, Susman JL: Managing musculoskeletal complaints with rehabilitation therapy: Summary of the Philadelphia Panel evidence-based clinical practice guidelines on musculoskeletal rehabilitation interventions. J Family Pract 51:1-7, 2002.

Table 49-2  The Rehabilitation Process 1. R  ecord the patient’s subjective information—in particular the primary complaint; document objective data to establish measurable baseline information. 2. Organize and interpret the assessment to identify primary deficits  and weaknesses. 3. Establish realistic short- and long-term goals, taking into consideration patient’s fitness and functional level prior to injury, severity of injury  or disability, and patient’s motivation. 4. Develop a treatment plan that incorporates rehabilitation  interventions—therapeutic exercise programs and modalities that  evidence has shown to be effective in the treatment of the patient’s injury or disability. 5. Use periodic measurements to assess progress, or the lack thereof, refining and/or modifying the treatment plan when needed. From Anderson MK, Hall SJ, Martin M: Sports Injury Management, 2nd ed.  Philadelphia, Lippincott Williams & Wilkins, 2000.

In 2007, Taylor and colleagues,2 whose review included results from the Philadelphia Panel, Smidt and colleagues and 36 other studies found strong evidence that therapeutic exercises can benefit people across broad areas of physical therapy practice.2 Reviews published in the years of 2002 to 2005 that were assessed by Taylor and colleagues2 showed that exercise interventions that led to significant improvements were varied and diverse, but all the effective exercise programs tended to be intense. These results were found in people with musculoskeletal disorders (e.g., people with chronic back pain and people who have had lumbar disc surgery). Similarly, people with multiple sclerosis, coronary heart disease, and COPD, who participated in programs four to five times a week at relatively high intensity, showed significant improvements in their muscle strength and mobility for those with multiple sclerosis and for patients with heart disease or COPD, improved exercise capacity and less shortness of breath. There was no evidence that exercise of relative intensity caused exacerbation of symptoms such as increased fatigue in patients with multiple sclerosis, or disc reherniation in patients who have had lumbar disc surgery.2 Another common theme that emerged was that results were more favorable when therapeutic exercise was compared to a no treatment control group. However, like Smidt and colleagues, Taylor and coworkers did not find sufficient evidence that one type of exercise was superior to another. This finding was common in many areas of practice.1,2 However, Taylor and colleagues noted that a particularly useful finding for clinical practitioners, was that therapeutic exercise may be more effective when it is individualized or targeted. Studies showed that individualized exercises were more effective than standardized exercise programs wherein every patient is given the same regimen.2 Effective individualized exercise programs begin with sequential steps to help identify the needs of the patient— assess the patient, interpret the assessment, establish goals, develop and supervise the treatment plan, and reassess the progress of the program (see Table 49-2).3 When assessment has been completed and documented, the individualized exercise program begins immediately.

The Neck The Evidence Neck pain accounts for billions of dollars each year in economic loss due to lost workdays, treatment and disability, with about 70% of the population experiencing an episode of neck pain at some

Table 49-3  Strength of Published Evidence and Clinical Recommendations of Previous Evidence-Based Clinical Practice Guidelines on the Use of Therapeutic Exercises for Acute Neck Pain Acute Neck Pain (<4 weeks)

Philadelphia Panel (2001)

Quebec Task Force (1987)

British Medical Journal (2000)

Quality of published evidence

NA

Common practice, but no evidence

NA

Listed as option to increase strength, ROM, and endurance

Good evidence that early mobilization, physical therapy,  and return to normal activity were more effective than rest  or immobilization for acute whiplash

Clinical recommendations

NA, not applicable; ROM, range of motion. Source: Philadelphia Panel Evidence-Based Clinical Practice Guidelines on Selected Rehabilitation Interventions for Neck Pain. Phys Ther 81:1701-1717, 2001.

Therapeutic Exercises  599

point in their lives. It is the second largest cause of time off from work, after low back pain. Acute neck pain is usually a result of injury or accident, most often road vehicle accidents associated with whiplash. Prognostic studies have suggested that chronic neck pain is associated with repetitive working conditions, and also with depression. Patient with neck pain are categorized into three widely accepted classifications: mechanical neck disorders (MND), including whiplash associated disorders, WAD), myofascial neck pain, and degenerative changes including osteoarthritis and cervical spondylosis; neck disorder with headache (NDH); and neck disorders with radicular findings (NDR). For these conditions, one of the most commonly used interventions is therapeutic exercise.6-8 In clinical practice, therapists use one or more types of exercise therapy, such as, active range of motion (AROM), stretching, strengthening, flexion or extension exercises, and proprioception exercises. AROM exercises are done by the patient and include active movement without resistance. Exercises could be gentle, active, small range, and amplitude movements or endrange sustained stretches. Strengthening exercises are any exercise done by the patient that includes resistance, such as isometric, isokinetic, or isotonic exercise. It could include strength training with machines, free weights, or low-load endurance exercises to train muscle control.6,8 Proprioception is a specialized variation of the sensory modality of touch that encompasses the sensation of joint movement. Proprioceptive exercises are performed with the goal of reducing the proprioceptive deficits.3 Gaining popularity among clinicians in the treatment of neck pain are spinal stabilization exercises. Examples of cervicothoracic stabilization exercises are shoulder shrugs, shoulder circles and squares, and scapular retraction.4 Rehabilitation specialists use concomitant treatment interventions within the same treatment session for a particular patient, such as mechanical traction, transcutaneous electrical nerve stimulation (TENS), and thermal therapy. Certain interventions, such as application of ultrasound and manual therapy are used for pain relief in the acute stage or as a treatment preparation before the main intervention.6 Table 49-3 outlines the strength of the evidence on the use of therapeutic exercises for acute neck pain. In its report of findings, the Philadelphia Panel found good scientific evidence (level I), with clinically important benefit on pain and function with supervised, isometric, or slow neck movement exercises. Based on the evidence, the panel recommends the inclusion of supervised exercise programs (including proprioceptive and traditional exercises) for the management of chronic neck pain. It was pointed out that the type of exercise, intensity, and progression needs to be clarified according to patient-specific classification of

physical dysfunction, needs, treatment goals, and outcomes. However, the panel’s review did not include studies on the efficacy of therapeutic exercises for acute or subacute conditions (Table 49-4).6 In another review, Kay and coworkers found limited evidence of benefit on active ROM exercises in whiplash-associated injuries. In studies assessing the use of strengthening exercises for subacute and chronic neck pain, two reviews found moderate evidence of benefit, with improvements in pain and function noted for patients with chronic neck with headache in the short and long term. The evidence on the use of strengthening exercises on patients with mechanical neck pain is unclear. The authors attributed this finding to several factors, including the location of focus of strengthening exercises and the types of strengthening exercises used in the studies that assessed the efficacy of strengthening exercises. However, Kay and colleagues did find moderate evidence of benefit on pain in chronic MND and NDH in the short term and long term when the stretching and strengthening program focused on the cervical or cervical and shoulder/thoracic region. In addition, a program of eye-fixation/proprioception exercises embedded in a complete exercise regimen shows moderate evidence of benefit for pain, function and global perceived effects for patients with chronic MND in the short term and on pain and function on patients with acute or subacute WAD with or without headache in the long term.7,8 Kay and coworkers also found strong evidence of benefit in a multimodal care approach of exercise combined with mobilizations or manipulations for subacute and chronic MND with or without headache in the short and long term. However, in the entire review, no explanation was given for this finding. The report did not specify if the benefit was for pain, function, or global perceived effect. Moreover, in the section on types of intervention that were included in this review, Kay and colleagues stated that studies were included if they used one or more type of exercise therapy, such as specific neck exercises, shoulder exercises, active exercise, stretching, strengthening and other types of exercise. The authors did not state that a multimodal approach that includes mobilization or manipulation would also be considered in the review.7 However, Gross and associates8 who reviewed conservative management of mechanical neck disorders, including mobilization and manipulation, did report strong evidence of benefit on pain, function, and perceived global effect with the use of the multimodal approach on patients with subacute and chronic MND, NDR, and NDH. Moffet and McLean4 found limited evidence for the use of any one specific exercise program and in evidence-based practice guidelines, no one specific program is recommended. Although the use of spinal stabilization exercises is gaining popularity in the treatment of neck pain, there is minimal evidence regarding its efficacy.4,7,8

Table 49-4  Strength of Published Evidence and Clinical Recommendations of Previous Evidence-Based Clinical Practice Guidelines on the Use of Therapeutic Exercises for Chronic Neck Pain Chronic Neck Pain (>12 weeks)

Philadelphia Panel (2001)

Quebec Task Force (1987)

British Medical Journal (2000)

Quality of Published Evidence

Good scientific evidence (level 1) for therapeutic exercise

Common practice, but no evidence

N/R

Clinical Recommendations

Good evidence (grade A for pain and function, grade B for patient global assessment) to include supervised therapeutic exercises

Listed as option to increase strength, ROM, and endurance

Insufficient evidence of effects of exercises in people with uncomplicated neck pain without neurologic deficit

N/R, not reported; ROM, range of motion. From Philadelphia panel evidence-based clinical practice guidelines on selected rehabilitation interventions for neck pain. Phys Ther 81:1701-1717, 2001.

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600  Physical Modalities for Pain Management

Guidelines for Stretching to Improve Flexibility

2. Levator Scapulae Stretching (Fig. 49-2)

1. Stretching is facilitated by warm body tissues; therefore, a brief warm-up period is recommended. If it is not possible to jog lightly, stretching could be performed after a superficial heat application. 2. In the designated stretch position, position yourself so a sensation of tension is felt. 3. Do not bounce; hold the stretch for 10 to 30 seconds until a sense of relaxation occurs. Be aware of the feeling of relaxation or “letting go”. Repeat the stretch six to eight times. 4. Breathe rhythmically and slowly. Exhale during the stretch. 5. Do not be overly aggressive in stretching. Increased flexibility may not be noticed for 4 to 6 weeks. 6. If an area is particularly resistant to stretching, partner stretching or proprioceptive neuromuscular facilitation may be used. 7. Avoid vigorous stretching of tissues in the following conditions: ll After a recent fracture ll After prolonged immobilization ll With acute inflammation or infection in or around the joint. ll With a bony block that limits motion ll With muscle contractures or when joint adhesions limit motion ll With acute pain during stretching

Selected Exercises 1. Trapezius Stretching (Fig. 49-1)

Figure 49-2  □

Sit or Stand Reach downward with right arm ll Turn head 45 degrees on the left side and look down ll Place your left hand on head and gently pull down ll Hold for 30 seconds and repeat three times in each direction ll ll

3. Scalenes Depressing Clavicle (Fig. 49-3)

Figure 49-1  □

Stand or Sit Reach downward with right arm ll Turn head to one side while pulling down gently to left stretching muscles on right side of the neck ll Hold for 30 seconds and repeat three times in each direction

Figure 49-3  □

Cross arm over chest Place hands over upper ribs and collar bone and firmly press downward toward stomach ll Tip head slightly to the side, turn and look up 45 degrees ll Hold for 30 seconds and repeat three times in each direction

ll

ll

ll

ll

Therapeutic Exercises  601

49

4. Stretch Rhomboids/Trapezius (Figs. 49-4 and 49-5)

Figure 49-6  □ ll ll

Figure 49-4  □

Bend neck sideways to left as you pull your right arm Hold for 30 seconds and repeat three times in each direction

The Back

Figure 49-5  □

Sit in a chair with erect posture, head held high Hands on top and middle of the thigh ll Then slowly bend forward, keeping arms straight, reaching to the floor ll Hold for 30 seconds and repeat three times ll ll

5. Stretch Upper Trapezius (Fig. 49-6) ll Place right arm behind back ll Grasp arm with left hand as shown

Low back pain is extremely common to all the industrial world. Sixty to 90% of the adult population is at risk of developing LBP at some point in their lifetime. Of those who develop acute LBP, 30% develop chronic LBP. Its high prevalence as well as its impact on functional ability usually leads to personal and socioeconomic consequences. It is the largest cause of workers’ compensation in the United States and Canada.9-12 The severity of LBP can range from an acute disabling problem to a chronic mild discomfort. Usually affected are joints, ligaments, discs, and capsule. Any damage to these primary structures may affect the nerve roots or spinal cord, and may lead to secondary muscle spasm, tightness, or weakness. As a result of direct injury to the back muscles, a pain-spasm cycle could also occur. Many nonpharmacologic therapies are available for the treatment of LBP, and in many cases, patients were referred to physical therapy for exercise therapy and other interventions.9-12 Because of the complexity and the number of variables involved, low back disorder and/or disability can be very difficult to assess accurately and treat successfully. Using the most widely accepted method of classification for LBP, where patients are categorized into one of three groups—serious spinal pathology, neurologic involvement, or nonspecific LBP, would help guide clinicians in the accurate assessment of LBP and thus, create and implement an effective treatment plan. Moreover, the clinician must watch for “red flags” during assessment, so if need be, a prompt referral to a specialist for further investigation can be arranged (Table 49-5).4 Nonspecific LBP is defined as pain between the gluteal fold and the uppermost lumbar vertebrae, including patients with postsurgery back pain. Because prognosis is typically dependent on the disease duration, nonspecific LBP is also classified into three widely accepted categories, acute (<4 weeks’ duration), subacute (4 to 12 weeks’ duration), and chronic (>12 weeks’ duration).11

602  Physical Modalities for Pain Management

Once red flags are ruled out and the patient assessment has been completed, the clinician must decide from among the various rehabilitation interventions that are available in the treatment of patients with nonspecific LBP. Among the most widely used intervention to treat nonspecific LBP is exercise therapy or therapeutic exercises. Exercise therapy encompasses a diverse mix of interventions that vary in type, intensity, frequency, and duration of exercise and the setting in which it is provided. Some of the more popular methods used are contradictory in theory and practice (Williams’ flexion and McKenzie’s extension exercises) and some have limited evidence in the literature.4,10,11 The Philadelphia Panel reviewed randomized controlled trials, nonrandomized controlled clinical trials or case control or cohort studies that evaluated therapeutic exercises and other rehab interventions in patients with nonspecific LBP. Outcomes weighed were functional status, pain, ability to work, patient global improvement, patient satisfaction, and quality of life.11 In its report, the panel found level I evidence that showed no clinically important benefit of stretching (including McKenzie) or strengthening exercises. The panel recommended there is poor evidence to include or exclude stretching or strengthening exercises alone as an intervention for acute LBP. This finding is consistent with other evidence-based guidelines, like the Compendium of the Best Available Evidence for Effective Health and the Agency for Health Care Policy and Research. However, the Quebec Task Force does recommend the prescription of general exercises as an option to increase strength, ROM, and endurance. In patients with subacute LBP, the Philadelphia Panel found good evidence to include extension, flexion and strengthening exercises as interventions (grade A for pain, function, and patient global improvement). For chronic LBP patients, the panel recommends stretching, strengthening, and mobility exercises. It found good scientific evidence (level I) that therapeutic exercises, in particular stretching and strengthening exercises, provided clinically important benefit for pain relief and functional status. In patients with postsurgery back pain, the panel found good evidence for strengthening and back extension exercises, with clinically significant improvements on pain and function.11 Table 49-5  Red Flags to Look for When Assessing Patients with Low Back Pain Age of onset <20 or >55 years Violent trauma Constant progressive, nonmechanical pain (no relief with bed rest) Thoracic pain Past medical history of malignant tumor Prolonged use of corticosteroids Drug abuse, immune deficiency disorders, human immunodeficiency  virus (HIV) Systemically unwell Unexplained weight loss Widespread neurologic conditions (including cauda equina syndrome) Structural deformity Fever From Moffet J, McLean S: The role of physiotherapy in the management of  non-specific back pain and neck pain. Rheumatology 45:371-378, 2006.

In a review commissioned by the American Pain Society and the American College of Physicians on nonpharmacologic therapies for LBP in adults, exercise therapy was found to be superior to usual care or no care for patients with acute LBP. There were no differences between exercise therapy and placebo or usual care for subacute LBP. For patients with chronic LBP, exercise therapy was associated with statistically significant but small effects on pain and function compared with other noninvasive interventions.12 In a review that considered 61 randomized, controlled trials to evaluate the effectiveness of exercise therapy in adults with nonspecific acute, subacute, and chronic LBP versus no treatment and other conservative treatments, analysis revealed no significant difference in short-term pain relief between exercise therapy and no treatment for acute LBP populations. Similarly, exercise therapy did not have a statistically significant positive effect on functional outcomes. In subacute LBP populations, evidence to support or refute the effectiveness of exercise therapy in reducing pain and improving function was deemed insufficient. However, it was noted that some evidence suggests that a graded-activity exercise program has some benefit in occupational settings. In chronic LBP patients, evidence strongly suggest that exercise is at least as effective as other conservative treatments, with statistically significant improvement in function and pain levels.13 In systematic reviews that assessed exercise therapy in general, and in those that studied specific types of exercise therapy and their efficacy in the treatment of LBP, findings are in agreement with the Philadelphia Panel, which found extension, strengthening, and flexion exercises effective for subacute and chronic LBP. A systematic review of McKenzie therapy concludes that the method results in greater decrease in pain and disability in the short-term than do other standard therapies. However, it was noted that there is insufficient data on long-term outcomes.14 In a study that compared the effects of spinal flexion and extension exercises on low-back pain severity and spinal mobility in patients with chronic LBP, it was reported that both the spinal flexion and spinal extension exercises provided significant reduction in LBP severity, with no statistically significant difference between treatment groups. In its conclusion, it was noted that both types of exercises can be used to reduce pain and increase spinal mobility.10 Alternatively, the efficacy of stabilization exercises alone or with other types of therapeutic exercises and rehab interventions in the treatment of nonspecific LBP is difficult to establish. A randomized controlled trial that evaluated the effect of stabilization exercises in reducing pain and disability, compared two patient groups, one received modalities, stretching and strengthening exercise, whereas the experimental group received stabilization exercises. The results revealed no statistically significant differences in reduction of pain intensity or increase of physical performance between both groups; however, there was a statistically significant difference between groups in the disability score in favor of the experimental group. However, the effect size was not reported. It must be noted that the sample size of the study is small (control, n = 20 and experimental, n = 20).15 An RCT studied the effectiveness of the Godelive Denys-Struft (GDS) method, which is based on the combination of individual manual therapy sessions and group sessions in which spinal stabilization exercises are performed along with exercises that work other muscles believed to help promote spinal stabilization, such as pelvic floor or diaphragm muscles. It was reported that at the end of the treatment sessions, the experimental group (GDS method) and the control group (conventional physiotherapy protocol) showed

Therapeutic Exercises  603

stabilization-enhanced general exercise approach with a general exercise-only approach. They found that the general exercise program reduced disability in the short term to a greater extent than a stabilization-enhanced exercise approach in patients with recurrent nonspecific LBP. They concluded that stabilization exercises do not appear to provide additional benefit to patients with subacute or chronic LBP who have no clinical signs suggesting the presence of spinal instability.17 In summary, there is strong evidence on the usefulness of flexion, extension, and strengthening exercises in reducing pain and improving function in patients with subacute and chronic back pain. Extension and strengthening exercises are effective on patients with postsurgery back pain. However, there is limited evidence on the usefulness of therapeutic exercises, in general, and specific types of exercises for patients with acute LBP (Tables 49-6 to 49-9). Additionally, the growing popularity of stabilization exercises by itself or in combination with other types of interventions

improvements in terms of three outcomes studied—pain, function, and quality of life. It also revealed that at follow-up 6 months after treatment, the control group had almost the same pain level as before treatment and also lost half of the improvements made in functional ability and quality of life. In its conclusion, it noted that the GDS method lead to greater improvements in the midterm in patient-perceived pain, functional ability, and quality of life than did the conventional treatment. However, it must be pointed out that the control group, defined as having received conventional physical therapy, actually received 15 sessions that consisted of the following: 14 40-minute sessions of TENS, plus 10 minutes of microwave treatment, and a single session in which patients were instructed on home exercises.16 Koumantakis and associates examined the usefulness of the addition of specific stabilization exercises to a general back and abdominal muscle exercise approach for patients with subacute or chronic nonspecific back pain by comparing a specific muscle

Table 49-6  Strength of Published Evidence and Clinical Recommendations of Previous Evidence-Based Clinical Practice Guidelines on the Use of Therapeutic Exercises for Acute Back Pain Acute Back Pain (<4 weeks)

Philadelphia Panel (2001)

Quebec Task Force (1987)

British Medical Journal (2000)

Quality of Published evidence

Good scientific evidence (level I) for light functional activities and therapeutic exercises

Common practice, but no evidence

N/R

Clinical Recommendations

Poor evidence to include or exclude flexion, extension, and strengthening exercises. Good evidence to include light functional activities, such as walking within first week of acute LBP

Listed as option to increase strength, ROM, and endurance

No evidence that flexion, extension,  aerobics, and strengthening are more  effective than other conservative interventions for acute LBP

LBP, low back pain; N/R, not reported; ROM, range of motion. From Philadelphia panel evidence-based clinical practice guidelines on selected rehabilitation interventions for low back pain. Phys Ther 81:1641-1674, 2001.

Table 49-7  Strength of Published Evidence and Clinical Recommendations of Previous Evidence-Based Clinical Practice Guidelines on the Use of Therapeutic Exercises for Subacute Low Back Pain Subacute Pain (4-12 weeks)

Philadelphia Panel (2001)

Quebec Task Force (1987)

British Medical Journal (2000)

Quality of published evidence

Good scientific evidence (level I) for therapeutic exercise

Common practice, but no evidence

Limited research-based evidence  (at least one adequate scientific study)

Clinical Recommendations

Good evidence (grade A for pain and function, grade B for patient global assessment) to include flexion, extension, strengthening exercises

Listed as option to increase strength, ROM, and endurance

Evidence does not support stretching exercises alone

ROM, range of motion. From Philadelphia panel evidence-based clinical practice guidelines on selected rehabilitation interventions for low back pain. Phys Ther 81:1641-1674, 2001.

Table 49-8  Strength of Published Evidence and Clinical Recommendations of Previous Evidence-Based Clinical Practice Guidelines on the Use of Therapeutic Exercises for Chronic Back Pain Chronic Back Pain (>12 weeks)

Philadelphia Panel (2001)

Quebec Task Force (1987)

British Medical Journal (2000)

Quality of published evidence

Good scientific evidence (level I) for therapeutic exercises

Usefulness demonstrated by nonrandomized controlled trial

N/R

Clinical Recommendations

Good evidence (grade A for pain and function) to include flexion, extension, and strengthening exercises

Listed as option to increase strength, ROM, and endurance

Good evidence that flexion, extension, aerobics, and strengthening are more effective than other conservative  interventions for chronic LBP

LBP, low back pain; N/R, not reported; ROM, range of motion. From Philadelphia panel evidence-based clinical practice guidelines on selected rehabilitation interventions for low back pain. Phys Ther 81:1641-1674, 2001.

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604  Physical Modalities for Pain Management

Table 49-9  Strength of Published Evidence and Clinical Recommendations of Previous Evidence-Based Clinical Practice Guidelines on the Use of Therapeutic Exercises for Postsurgery LBP (4-12 weeks) Postsurgery LBP (4-12 weeks)

Philadelphia Panel (2001)

Quebec Task Force (1987)

British Medical Journal (2000)

Quality of published evidence

Good scientific evidence (level I) for therapeutic exercises

N/R

N/R

Clinical recommendations

Good evidence (grade A for pain and function)  to include extension and strengthening exercises

N/R

N/R

N/R = not reported. From Philadelphia panel evidence-based clinical practice guidelines on selected rehabilitation interventions for low back pain. Phys Ther 81:1641-1674, 2001.

in clinical practices is not supported by evidence in the literature. More methodologically-sound randomized controlled trials are needed on the use of stabilization exercise for patients with nonspecific LBP.

Selected Exercises Assisted Hamstring Stretching (Fig. 49-7) Figure 49-9  □

Straighten legs and place heels on apex of ball Co-contract gluteals and abdominals while maintaining “neutral” spine (slight lordosis) and bridge the pelvis up ll Hamstring curl basic exercise: When this elevated position can be held stable for a few repetitions, pull the ball toward buttocks with the heels by flexing the knees Progression ll Advanced hamstring curl: Start with knees flexed almost 90 degrees ll Bridge up and pull heels closer to buttocks ll Lower and return to start position ll Progress further by performing single leg hamstring curl in each of these positions as shown. (Figs. 49-10 to 49-13). ll ll

Figure 49-7  □

Patient in supine position Hip flexed and knee extended on involved limb ll Hip and knee extended on the table on nontreated side ll Perform one set of three repetitions ll Hold exercise for 30 seconds ll ll

Care should be taken when stretching the hamstrings, especially in cases where sciatic nerve tension tests are negative. Also, if you suspect a case of lumbar joint irritability, the opposite hip and knee may be flexed to reduce strain on the lumbar spine. Hamstring Curls (Figs. 49-8 and 49-9)

Figure 49-10  □

Figure 49-8  □

Figure 49-11  □

Therapeutic Exercises  605

Lie on back with knees bent, feet flat on table Maintain neutral position ll Lift buttocks off table ll Lift and straighten left knee Resist Lumbar Bridging (Fig. 49-16) ll ll

Figure 49-12  □

Figure 49-16  □

Lie on back with knees bent Loop elastic band around lower thighs ll Raise buttocks up and hold ll Move knees apart, then together ll Lower buttocks and repeat ll Perform one set of three repetitions ll Hold exercise for 30 seconds ll ll

Figure 49-13  □

Bridging Exercises (Fig. 49-14)

This can be performed without a band, but to target the gluteus maximus and medius, add resistance to thigh abduction and external rotation manually or with a band Lumbar Bridging Bilateral on Ball (Figs. 49-17 and 49-18)

Figure 49-14  □

Supine, hook-lying position (feet under knees) Slightly externally rotate thighs ll Squeeze the gluteals and slowly raise pelvis up Progression ll Perform single leg bridge in an isometric manner by maintaining bridge while alternating lower leg raise ll Perform single leg bridge in an isotonic manner by bridging up and down on one leg. ll AROM Lumbar Bridging with Static Knee Extension (Fig. 49-15) ll ll

Figure 49-17  □

Figure 49-18  □

Lie on back with knees bent over ball as shown Lift buttocks off floor ll Hold for 5 seconds ll Return to start position ll Repeat 10 times ll ll

Figure 49-15  □

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606  Physical Modalities for Pain Management

AROM Lumbar Rotation with Ball (Fig. 49-19)

Sit with the right knee bent, right ankle to outside of left leg Grasp knee and pull thigh across chest toward left shoulder ll Relax and repeat with left leg ll Perform one set of three repetitions ll Hold exercise for 30 seconds Piriformis Self-Stretching (Fig. 49-22) ll ll

Figure 49-19  □

Lie on back with both feet on the ball as shown Slowly twist at waist, moving ball to left and right ll Repeat 10 times to each side Piriformis Stretching—Supine (Fig. 49-20) ll ll

Figure 49-22  □

Sit with the involved leg on the top Lean forward until stretch is felt in the buttocks ll Hold exercise for 30 seconds and relax ll Repeat five times Posterior Hip Capsule and Piriformis Stretching (Fig. 49-23 to 49-25). ll ll

Figure 49-20  □

Lie on back Lift involved leg to chest and grasp knee with opposite hand ll Grasp lower calf with your other hand ll Gently pull your leg across chest to opposite shoulder while rotating leg inward until a stretch is felt deep in the buttocks ll Perform one set of three repetitions ll Hold exercise for 30 seconds Piriformis Stretching—Long Sitting (Fig. 49-21) ll ll

Figure 49-23  □

Figure 49-21  □

Figure 49-24  □

Therapeutic Exercises  607

Perform one set of three repetitions Hold exercise for 30 seconds Iliopsoas Self-Stretches (Fig. 49-28)

ll ll

Figure 49-25  □

Iliopsoas Stretching in Supine Position(Fig. 49-26).

Figure 49-26  □

Supine with the uninvolved leg hanging off edge of bed Involved hip and knee held in full flexion against chest ll Lumbar spine may be laterally flexed away from the psoas being treated ll Perform one set of three repetitions ll Hold exercise for 30 seconds Iliopsoas Stretching in Side-Lying Position(Fig. 49-27)

Figure 49-28  □

Standing Involved leg elevated using a chair ll Keep the other leg extended and gently lean forward to feel the stretch ll Hold exercise for 30 seconds ll Repeat five times

ll

ll

ll

ll

Self-Stretches It is important when performing self-stretches for the hip flexors that the stretch is felt in the anterior hip or thigh and not in the low back. For the iliopsoas, this is best accomplished if the patient holds a posterior pelvic tilt and internally rotates the hip while stretching. Rectus Femoris and Quadriceps Stretching (Figs. 49-29 to 49-31) Half kneel ll Flatten back by tightening abdominal muscles ll Lean forward slowly keeping hips and back straight until a stretch is felt in outside of right thigh ll Hold exercise for 10 seconds and repeat five times ll Perform for the left leg Progression 1 ll Half kneel with left foot elevated with a stool as shown Progression 2 ll Progress by grasping with a hand and gently pull up toward buttocks ll The rectus femoris stretch requires some knee flexion and the ability of the patient to produce and maintain a braced lumbar spine ll

Figure 49-27  □

Lie on your side (side-lying), involved side up Nontreated leg bent at knee and hip ll Thigh abducted (knee flexed to isolate adductors) until resistance is felt. ll ll

49

608  Physical Modalities for Pain Management

Stretch Lumbar with Rotation (Fig. 49-32)

Figure 49-29  □

Figure 49-32  □

Standing Place right foot on a chair or stool ll Grasp right knee with left hand ll Gently pull with left arm and twist trunk to the right ll Hold exercise for 10 seconds ll Relax and repeat 10 times ll Repeat stretch to the left foot on chair Erector Spinae Assisted Stretching (Fig. 49-33) ll ll

Figure 49-30  □

Figure 49-33  □

Lie on back, with knees bent Therapist gently push knee to chest with facilitation given on patient’s hip ll Hold exercise 30 seconds and repeat five times AROM Lumbar Extension Prone High Level (Fig. 49-34) ll Lie face down with arms outstretched over the side ll Arch upward, raising arms and legs off floor ll Return to start and repeat 10 times ll ll

Figure 49-31  □

Therapeutic Exercises  609 ll ll

Keep low back straight Return to start position and repeat Special Instructions ll Keep low back straight and abdominal muscles tight ll Perform two sets of five repetitions.

The Knee Figure 49-34  □

Lumbar Stabilization (Figs. 49-35 and 49-36)

Figure 49-35  □

Figure 49-36  □

Kneel in upright position with buttocks on heels Hold weights in hands ll Arms begin at sides ll Lift arms up and to front while lifting up off buttocks and leaning forward with trunk ll ll

Chronic knee pain is one of the most common reasons for visits to a family practitioner. Acute knee pain usually follows injury or surgery. Chronic knee pain can be related to a disease such as osteoarthritis or associated with overuse or untreated injuries to muscles, ligaments, or tendons. Several etiologies of knee pain exist—chondromalacia patellae (patellofemoral pain syndrome), postsurgical conditions, and osteoarthritis.18 Osteoarthritis (OA) is the most common form of arthritis in Western populations. It primarily affects the articular cartilage and subchondral bone of a synovial joint and results in joint failure. Radiographic features are the formation of osteophytes at the joint margins, joint space narrowing, subchondral sclerosis, subchondral cyst formation, and chondrocalcinosis. It has been estimated that 40% to 80% of people with these radiographic changes will have symptomatic OA, especially in people older than 55 years. People with symptomatic OA of the knee complain of deep, aching pain. In early stages, pain is intermittent and mostly associated with joint use. As the disease progresses, the pain becomes more chronic and may also be present at rest and during the night, with the joint feeling stiff after a period of rest, resulting in pain and difficulty initiating movement. Patients may also experience crepitus or deep creaking sounds on movement and ROM often becomes limited, causing patients with the disease to experience increased difficulty and disability in walking, stair-climbing, and other daily functional activities. Physical disability arising from pain and loss of functional capacity reduces quality of life and increases the risk of further morbidity.19,20 Patellofemoral pain syndrome (PFPS) is a common complaint in adolescents and young adults. The symptom most frequently reported is a diffused peripatellar (around the knee cap) and retropatellar (behind the knee cap) localized pain, typically provoked by ascending or descending stairs, squatting and sitting with flexed knees for prolonged periods of time. Other common symptoms are crepitus and giving-way. However, the cause of PFPS is complicated, with several factors implicated.21 The European League Against Rheumatism (EULAR), in its 2003 recommendations on the management of knee osteoarthritis recommended that the treatment of knee OA should be tailored according to: knee risk factors (obesity, adverse mechanical factors, physical activity), general risk factors (age, comorbid conditions, polypharmacy), level of pain intensity and disability, sign of inflammation (effusion), and location and degree of structural damage. EULAR also reported that the optimal management of knee OA requires a combination of nonpharmacologic and pharmacologic treatment modalities.19 Current nonpharmacologic treatments for OA of knee and patellofemoral pain syndrome, as well as for patients who underwent knee arthroplasty, include a variable number of sessions of physical therapy.18-21 The therapist will use specific evaluative tools to determine an optimal treatment plan. These tools include: patient medical history and lifestyle, including occupational and leisure activities; sensory evaluation to determine presence of any pain or sensory loss; assessment of ROM, both passive and active to determine malalignment, laxity or tightness; measuring circumference at the knee to assess the presence of edema and atrophy; assessing quadriceps

49

610  Physical Modalities for Pain Management

control for indications of muscle strength, evaluating gait patterns, which may reveal reduced motor control and assessing functional activities.22 The therapists will use various rehab interventions during treatment, but a major component will be therapeutic exercises. The aim of therapeutic exercises is to improve functional status by increasing muscle strength, improving flexibility, and reducing pain.18 The application of specific types of exercises, intensity and duration will depend on the patient’s unique circumstances, the goals of the treatment program, and other major factors.18,22 These factors include quadriceps inhibition or activation failure, obesity, passive knee laxity, knee alignment, fear of physical activity, and self-efficacy. The literature suggests that the inability of therapeutic exercises to address some of these factors might place barriers on the patient’s ability to achieve maximum benefits from a rehabilitation program.18,19,20 Of major concern throughout the rehabilitative process of any knee problem is the maintenance or improvement of quadriceps control. The quadriceps, like most muscles, are composed of both tonic and phasic extrafusal muscle fibers. The tonic fibers have a low threshold to stimulation and do not easily fatigue; however, these fibers tend to atrophy after prolonged immobilization or inactivity, resulting in an inability of the quadriceps to sustain an isometric contraction in the shortened range. The initial focus of treatment in such cases is to enhance the isometric activity by facilitating a shortened held resisted contraction. In patients with knee osteoarthritis, who have reduced functional performance, therapeutic exercises are thought to compensate for the arthrogenic impairment in the quadriceps femoris muscle sensorimotor function, improve diminished proprioceptive acuity, and increase postural stability.18 In patients with PFPS, resisted movement through range may aggravate this condition, whereas increased control of the vastus medialis is usually indicated and can be promoted by resisted isometric contractions in the shortened range of knee extension.21,22 Patients who have undergone surgical repair may require prolonged immobilization. In these cases, rotational motions of the knee are not indicated during the first stages of treatment.22 Pain is another major concern during the initial treatments. Procedures are always performed within the patient’s pain tolerance to prevent further trauma to the tissues. An increase in pain is usually indicative of an increase in stress to the inert or contractile tissues. Extra caution must be taken during ROM and strengthening exercises to prevent trauma.22 The exercise procedures are divided into three stages: initial, middle, and advanced. Depending on each patient’s unique circumstances, the therapist may begin ROM exercises or quadriceps control exercises. Increasing movement into knee flexion is also a goal of treatment and is promoted following the increasing of range into extension and the enhancement of quadriceps control. At the middle stage, postsurgery patients will have achieved full passive motion into extension and knee flexion to at least 90 degrees. For nonsurgical patients, for example, those with PFPS or knee OA, treatment may begin at this stage. At this point, isometric control in shortened range of knee extension is emphasized for all patients, with focus on direct activation of the quadriceps with a progressive increase in the amount of resistance. These activities will increase quadriceps isometric control, further increase ROM and increase power, strength, and endurance of the quadriceps and hamstrings. During the advanced stage, the patient should have good strength of the quadriceps and hamstrings and little difficulty with terminal extension. Strengthening exercises also improve gait and attenuate knee pain in activities of daily living among patients with osteoarthritis. At this point, the goals are to promote normal functional ability, improve eccentric control of the quadriceps, and promote advanced stages of motor control.18,22

However, because there are many causes to knee dysfunction and each patient reacts differently to even the same disability, the treatment program should be developed according to the individual needs, goals, and specific problems. In addition to the patients’ individual needs, the therapist must also consider the current literature on the usefulness of rehabilitation interventions in the treatment of the various knee dysfunctions. For patients with PFPS, a systematic review of studies on the efficacy of therapeutic exercises, found evidence that suggests that exercise is effective, but the pooled results of the relevant studies are not straightforward, with some studies suggesting that exercise therapy provides significant pain reduction, whereas one study contradicts this finding. Regarding the improvement in function, two studies found no improvement, whereas one low-quality RCT reported positive results.21 The Philadelphia Panel found that there are insufficient data to support or refute the efficacy of therapeutic exercises for patellofemoral pain syndrome.18 However, there is sufficient evidence to support the efficacy of closed and open kinetic chain exercises for pain reduction and improved function.21 For patients who received exercise therapy after knee surgery, there is some evidence of its usefulness in reducing pain and improving function. A systematic review of the effectiveness of exercise therapy after knee arthroplasty found sufficient evidence to support the efficacy of functional exercises for improved function. The pooled results of the studies considered in the review found small to moderate standardized effect size in improved function over 3 to 4 months postoperatively and improved ROM and quality of life over the same period. However, none of the benefits were seen 1 year after surgery. It was noted that improved function is an important outcome in clinical practice, possibly more important than ROM, which is affected by factors beyond the therapists’ control, such as prosthetic design, preoperative knee motion, and surgical technique.23 RCTs that compared other rehab interventions with exercise therapy found that the control groups (exercise group) exhibited the same positive results as the experimental groups.24,25 Beaupre and colleagues (2001) found that all three groups—the exercise group, the CPM group, and the slider board group exhibited improved ROM in knee flexion and extension, with no statistically significant difference among groups; similarly, in patient-reported outcomes all three groups reported improvement in terms of pain, stiffness, and function.24 Similarly, Denis and coworkers found that adding CPM devices to exercise therapy did not have any additional benefit on active ROM in knee flexion or on any of the other secondary outcomes measured (ROM in knee extension, patient-reported pain, stiffness, and function).25 Exercise therapy for patients with knee osteoarthritis has strong evidence in the literature to support its application. The Philadelphia Panel found level I evidence that showed clinically important benefit of strengthening exercises on knee osteoarthritis pain. Its recommendation states that there is good evidence to include strengthening, stretching, and functional exercises for pain and patient global assessment.18 Similarly, a review of therapeutic exercises for people with knee OA concluded that there is platinum level evidence on the effectiveness of land-based therapeutic exercises relative to patient-reported outcomes. In its report of findings, land-based therapeutic exercises demonstrated small, but significant, benefits in terms of knee pain and physical function.20 A large-scale review of physical therapy interventions found high-quality evidence that therapeutic exercises reduce pain and improve function in patients with knee OA. It found therapeutic exercises to be effective in reducing pain and improving function. It also found that aerobic exercises and other exercises that promoted weight loss improved disability in patients with weight issues.26

Therapeutic Exercises  611

49

The literature has sufficient data on usefulness of therapeutic exercises in patients with chronic knee pain, in particular, knee osteoarthritis, where the RCTs are typically of high quality. More research is needed on efficacy of therapeutic exercises for patients with patellofemoral pain syndrome and postsurgery knee patients. However, the Philadelphia Panel and other authors noted that in all studies on knee disability, the types of exercises, intensity, and progression need to be clarified according to physical dysfunction, needs, treatment goals, and outcomes. Also recommended is the need for an enormous research effort on rehabilitation interventions for knee pain, for prospective RCTs to identify predictors of patient responsiveness to therapeutic exercises, for multi-armed placebo-controlled RCTs to identify the optimal types of exercise and dosage for each type of knee dysfunction.18,20

Selected Exercises AROM Knee Wall Slide Bilateral (Fig. 49-37)

Figure 49-38  □

Place involved leg on edge of step Step up, lifting uninvolved leg off floor ll Lower uninvolved foot toward floor but do not touch floor. ll Step up again and continue ll Perform three sets of 10 repetitions ll Rest 1 minute between sets ll Perform one repetition every 4 seconds Isometric Knee Squat (Figs. 49-39 and 49-40) ll Stand on balance board, feet at hip distance apart or closer ll Slightly bend knees and hold ball in front at waist height ll Raise ball overhead ll Lower and repeat ll Perform one set of 10 repetitions ll Hold exercises for 10 seconds Knee Squats with Dumbbell (Fig. 49-41) ll Place dumbbell over shoulders, behind head ll Grip bar firmly with hands, elbows bent to 90 degrees ll Feet should be about shoulder distance apart ll Slowly bend knees, keeping back straight ll Return to start position and repeat ll Perform one set of 10 repetitions ll Start with light weight and increase as patient tolerates Resist Knee Squat (Figs. 49-42 and 49-43) ll Stand on both legs ll Hold weights in both hands ll Bend knees to 90 degrees ll Straighten knees ll Repeat and perform one set of 10 repetitions Progression ll Stand on the involved leg ll Hold weights in both hands ll Bend knee to at least 90 degrees and straighten knee ll ll

Figure 49-37  □

Place ball between back and wall Slowly bend knees to 90 degrees ll Hold for 5 seconds, and return to standing position. ll Repeat 10 times Advantages of Closed Kinetic Chain Exercises ll It provides greater joint compressive forces ll Multiple joints are exercised through weight bearing and ­muscular contractions ll Velocity and torque are more controlled ll Shear forces are reduced ll Joint congruity is enhanced ll Proprioceptors are reeducated ll Postural and dynamic stabilization mechanics are facilitated ll Exercises can work in spiral or diagonal movement patterns AROM Knee Step Up/Down Lateral Partial (Fig. 49-38) ll ll

612  Physical Modalities for Pain Management

Figure 49-39  □

Figure 49-40  □

Figure 49-41  □

Figure 49-42  □

Therapeutic Exercises  613

Figure 49-43  □

The Hip The hip is the second most common large weight-bearing joint to be affected by osteoarthritis (OA), a chronic joint condition characterized by pain, disability, and impairment. The prevalence of hip OA ranges from 3% to 11% in Western populations more than 35 years of age. It is often associated with significant pain, disability, and impaired quality of life. Main treatment goals are improving function, relieving symptoms, and improving quality of life. The optimal management of hip OA requires a combination of nonpharmacologic and pharmacologic treatment modalities. Physical rehabilitation interventions, including therapeutic exercise, is recommended.27,28 Exercise therapy aims to improve the patients’ overall function and to help them meet the demands of daily living. Because exercise therapy can vary in content, dosage, and mode of delivery, the therapist must base decisions on clinical judgment.28 The EULAR taskforce recommends that the following factors should be considered: hip risk factors (obesity, adverse mechanical factors, physical activity, dysplasia); general risk factors (age, sex, comorbid conditions, comedication) level of pain intensity, disability, and handicap; location and degree of structure damage; and wishes and expectations of the patient. The taskforce reports that these clinical markers used to guide clinical decisions are based on expert opinion and standard clinical practice only because there are no appropriate clinical trials to support the recommendation.27 Several reviews have found evidence on the usefulness of exercise therapy in hip OA to be limited. Although literature search yielded many results, most of the existing reviews studied knee and hip OA. The EULAR report points out that although available treatments for hip osteoarthritis are similar to knee OA, there are certain differences because the effect size of a specific treatment might vary according to the site of the OA involvement, owing to

differences in anatomy, biomechanics, risk factors for development and progression, and accessibility to local treatments.27 Despite the paucity of evidence, the EULAR taskforce still recommends the use of exercise therapy in the treatment of hip OA, citing clear face-validity and expert opinion, as well as strong evidence of the usefulness of therapeutic exercises in other types of OA.27 Roddy and coworkers reported that there is insufficient data to conclude that strengthening exercises could reduce pain and improve function in people with hip OA.29 Pisters and colleagues, who studied the long-term effectiveness of exercise therapy in patients with hip or knee OA, reported strong evidence for no long-term effect on pain and self-reported function. However, it did report that moderate evidence exists for the effectiveness of additional posttreatment booster sessions in terms of long-term observed physical function. It must be noted that in its report of findings, the authors did not make the distinction between knee or hip OA.30 An umbrella review of nonpharmacologic and nonsurgical interventions, reported that there is insufficient evidence to make conclusions about the effect of exercise therapy on pain, disability, or health status.28 Roddy and colleagues also reported that there is no evidence in the literature to suggest that individualized, patient-centered exercise therapy is any more effective than group sessions. However, it was noted that although evidence may not support the practice, because RCTs tend to recruit homogeneous populations to whom standardized interventions are delivered with little room for individualization, individualized, patient-centered exercise regimens still have clear face-validity and are recommended in clinical guidelines.29

Selected Exercises Stretch Piriformis—Sitting (Figs. 49-44 and 49-45)

Figure 49-44  □

Begin sitting on the floor/table Involved leg in front ll Lean forward and toward involved side until stretch is felt on buttocks ll Hold for 30 seconds and return to original position ll Repeat exercise five times Proprioceptive Exercises for Hip and Knee Using Trampoline (Figs. 49-46 and 49-47) ll Stand on mini trampoline ll Slowly begin to lift leg/alternating with the other leg ll Make sure to maintain upright posture while performing the exercise ll ll

49

614  Physical Modalities for Pain Management

Figure 49-45  □

Figure 49-47  □

Figure 49-48  □

The Shoulder Figure 49-46  □

Stay in center of the trampoline Perform 10 repetitions each leg Progression ll Slowly begin to jump up and down with both feet ll Keep feet about shoulder distance apart ll Start slowly and keep jumps low Closed Chain Knee Exercise (Fig. 49-48) ll Lie on back, involved knee bent, foot on wall, as shown ll Place ankle of uninvolved leg over the other leg ll Slowly press down, bending knee toward the floor ll Perform one set of five repetitions ll ll

The prevalence of shoulder pain accompanied by disability is approximately 20% in the general population. Conditions causing shoulder pain are common and contribute substantially to the musculoskeletal morbidity of the community. The shoulder is frequently injured in sports, and prevalence and disability tend to increase in age, the peak prevalence occurring in the 56 to 60 year age group.31,32 Shoulder disorders often result in substantial disability. ­Moving the shoulder allows for hand placement, therefore compromised shoulder mobility significantly affects ability to perform tasks of daily living. Moreover, shoulder pain is known to affect one’s ability to sleep. People with shoulder pain tend to score significantly higher than normal values in standardized tests that measure physical, social and emotional function, and pain. Most patients diagnosed with shoulder pain are referred to physical therapy.32

Therapeutic Exercises  615

Physical therapy encompasses a broad range of interventions. The aim is to relieve pain, promote healing, reduce muscle spasms, increase joint range and strengthen weakened muscles, and, ultimately, to prevent and treat functional impairment.31,32 However, the Philadelphia Panel found the data on therapeutic exercises for shoulder pain to be insufficient. A systematic review of physical therapy interventions conducted in 2003, reported that supervised exercise therapy demonstrated significant benefit in the short and long term. In its report of findings, it was not indicated if the benefits were in terms of pain and/or function.31,32 Existing reviews noted the urgent need for more RCTs to determine whether therapeutic exercises are effective at reducing pain and improving long-term patient-important outcomes. It was noted that existing RCTs studied populations with mixed diagnoses (rotator cuff disease, adhesive capsulitis, calcific tendonitis). Studies often compared various interventions with other interventions, instead of using placebo as control group.31,32 The state of current research and the paucity of evidence on the efficacy of therapeutic exercises in the treatment of shoulder pain offer significant clinical challenge to practitioners. A good clinician must be able to choose appropriate interventions to produce optimal treatment outcomes, and with no sufficient evidence in the literature, must rely on clinical experience and training to develop individualized, patient-­centered exercise regimens.

Begin lying face down (prone position), propped up on elbows Grasp elastic in both hands and pull outward ll Return to start position and repeat ll Perform two sets of five repetitions Shoulder Stabilization (Figs. 49-51 and 49-52) ll ll

Selected Exercises Anterior Glide of the Shoulder Joint (Fig. 49-49) Figure 49-51  □

Figure 49-49  □

Lie on back with trunk supported on elbows Relax shoulder muscles, leaning between arms ll Perform 1 set of 10 repetitions. Shoulder External Rotation with Resistance (Fig. 49-50) ll ll

Figure 49-52  □

Hold a ball against the wall Keep elbow straight and push firmly on ball ll Slowly lower body to the ball keeping the ball steady during the push up ll ll

Figure 49-50  □

49

616  Physical Modalities for Pain Management ll

Perform two sets of five repetitions Progression ll Use balance board as shown and perform the same procedure. (Figs. 49-53 and 49-54)

Figure 49-55  □

Figure 49-53  □

Figure 49-56  □

Figure 49-54  □

Push Up with Ball (Figs. 49-55 and 49-56) Position body on floor with hands on ball, elbows straight as shown ll Slowly lower body to floor and return to starting position ll Keep ball steady during the push up ll Perform two sets of five repetitions Shoulder Push-Ups Kneel with Balance Board (Figs. 49-57 and 49-58) ll Position body on floor with hands on balance board, elbows straight as shown ll Slowly lower body to floor and return to starting position ll Keep board steady during the push up ll Perform two sets of five repetitions

Figure 49-57  □

ll

Figure 49-58  □

Therapeutic Exercises  617

REFERENCES   1. Smidt N, de Vet HC, Bouter LM, et al. Effectiveness of exercise therapy: a best-evidence summary of systematic reviews. Aust J Physiother. 2005;51:71-85.   2. Taylor NF, Dodd KJ, Shields N, Bruder A. Therapeutic exercise in physiotherapy practice is beneficial: a summary of systematic reviews 2002-2005. Aust J Physiother. 2007;53:7-16.   3. Anderson MK, Hall SJ, Martin M. Sports Injury Management. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2000.   4. Moffet J, McLean S. The role of physiotherapy in the management of non-specific back pain and neck pain. Rheumatology. 2006;45:371-378.   5. Harris GR, Susman JL. Managing musculoskeletal complaints with rehabilitation therapy: summary of the Philadelphia Panel evidencebased clinical practice guidelines on musculoskeletal rehabilitation interventions. J Fam Pract. 2002;51:1042-1046.   6. Philadelphia panel evidence-based clinical practice guidelines on selected rehabilitation interventions for neck pain. Phys Ther. 2001;81: 1701-1717.   7. Kay TM, Gross A, Goldsmith CH, et al. Exercises for mechanical neck disorders. Cochrane Database of Syst Rev. 2005(Issue 3).   8. Gross AR, Goldsmith C, Hoving JL, et al. Conservative management of mechanical neck disorders: a systematic review. J Rheumatol. 2007;34: 1083-1102.   9. Hayden JA, van Tulder MW, Tomlinson G. Systematic review: strategies for using exercise therapy to improve outcomes in chronic low back pain. Ann Intern Med. 2005;142:776-785. 10. Elnaggar IM, Nordin M, Sheikhzadhe A, et al. Effects of spinal flexion and extension exercises on low-back pain and spinal mobility in chronic mechanical low-back pain patients. Spine. 1991;16:967-972. 11. Philadelphia Panel evidence-based clinical practice guidelines on selected rehabilitation interventions for low back pain. Phys Ther. 2001;81: 1641-1674. 12. Chou R, Huffman LH. Nonpharmacologic therapies for acute and chronic low back pain: a review of the evidence for an American Pain Society/American College of Physicians clinical practice guideline. Ann Intern Med. 2007;147:492-504. 13. Hayden JA, van Tulder MW, Malmivaara AV, Koes BW. Metaanalysis: exercise therapy for nonspecific low back pain. Ann Intern Med. 2005;142:765-775. 14. Clare HA, Adams R, Maher CG. A systematic review of efficacy of McKenzie therapy for spinal pain. Austr J Physiother. 2004;50:209-216. 15. Ali TA. Stabilization exercises for patients with low back pain 54 2006. (The Cochrane Controlled Trials Register [CCTR/CENTRAL]). In The Cochrane Library. Oxford: Update Software; 2009, Issue 1, Updated quarterly. 16. Dîaz Arribas MJ, Ramos Sånchez M, Pardo Hervås P, Løpez P, et al. Effectiveness of the physical therapy Godelive Denys-Struyf method for nonspecific low back pain: Primary care randomized control trial. Spine. 2009;34:1529-1538. 17. Koumantakis GA, Watson PJ, Oldham JA. Trunk muscle stabilization training plus general exercise versus general exercise only: randomized controlled trial of patients with recurrent low back pain. Phys Ther. 2005;82:209-225.

18. Philadelphia Panel evidence-based clinical practice guidelines on selected rehabilitation interventions for knee pain. Phys Ther. 2001;81: 1675-1700. 19. Jordan KM, Arden NK, Doherty M, et al. EULAR recommendations 2003: an evidence based approach to the management of knee osteoarthritis: Report of a Task Force of the Standing Committee for International Clinical Studies Including Therapeutic Trials (ESCISIT). Ann Rheum Dis. 2003;62:1145-1155. 20. Fransen M, McConnell S. Exercise for osteoarthritis of the knee. Cochrane Database Syst Rev. 2008: Issue 4. Art. No.: CD004376. DOI: 10.1002/14651858.CD004376.pub2. 21. Heintjes EM, Berger M, Bierma-Zeinstra SMA, et al. Exercise therapy for patellofemoral pain syndrome. Cochrane Database of Systematic Reviews. 2003: Issue 4. Art. No. CD003472. DOI: 10.1002/14651858. CD003472. 22. Sullivan PE, Markos PD, Minor MA. An Integrated Approach to Therapeutic Exercise. Theory and Clinical Application. Reston, VA: Reston Pub. Co.; 1982. 23. Minns-Lowe CJ, Barker KL, Dewey M, Sackley CM. Effectiveness of physiotherapy exercise after knee arthroplasty for osteoarthritis: systematic review and meta-analysis of randomized controlled trials. BMJ. 2007;335:812. 24. Beaupré LA, Davies DM, Jones CA, Cinats JG. Exercise combined with continuous passive motion or slider board therapy compared with exercise only: a randomized controlled trial of patients following total knee arthroplasty. Phys Ther. 2001;81:1029-1037. 25. Denis M, Moffet H, Caron F, et al. Effectiveness of continuous passive motion and conventional physical therapy after total knee arthroplasty: a randomized clinical trial. Phys Ther. 2006;86:174-185. 26. Jamtvedt G, Dahm KT, Christie A, et al. Physical therapy interventions for patients with osteoarthritis of the knee: an overview of systematic reviews. Phys Ther. 2008;88:123-136. 27. Zhang W, Doherty M, Arden N, et al. EULAR evidence-based recommendations for the management of hip osteoarthritis: report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2005;64: 669-681. 28. Moe RH, Haavardsholm EA, Christie A, et al. Effectiveness of nonpharmacological and nonsurgical interventions for hip osteoarthritis: an umbrella review of high-quality systematic reviews. Phys Ther. 2007;87:1716-1727. 29. Roddy E, Zhang W, Doherty M, et al. Evidence-based recommendations for the role of exercise in the management of osteoarthritis of the hip or knee—the MOVE consensus. Rheumatology. 2005;44:67-73. 30. Pisters MF, Veenhof C, Meeteren NLU, et al. Long-term effectiveness of exercise therapy in patients with osteoarthritis of the hip or knee: A systematic review. Arthritis Rheum. 2007;57:1245-1253. 31. Philadelphia Panel evidence-based clinical practice guidelines on selected rehabilitation interventions for shoulder pain. Phys Ther. 2001;81:1719-1730. 32. Green S, Buchbinder R, Hetrick SE. Physiotherapy interventions for shoulder pain. Cochrane Database Syst Rev. 2003 Issue 2. Art. No. CD004258. DOI: 10.1002/14651858.

49

Index

A Abscess(es) epidural complicating selective spinal injections, 39, 39f complicating spinal cord stimulation, 483 paraspinal, complicating selective spinal injections, 39f Accounts receivable follow-up, 56 Achilles bursitis, injections for, 80 Achilles tendinopathy, prolotherapy for, 124 Achilles tendon sheath, corticosteroid ­injections in, 86 Achillobursitis, injections for, 80 Acromioclavicular joint, corticosteroid injections in, 66–67, 66f–67f Active release technique, 578 Acupressure massage, 579 Acupuncture Chinese scalp, 173 clinical applications of, 179–185 for complex regional pain, 179–180 case report on, 180 contraindication and precaution for, 179 for fibromyalgia, 182 case report on, 182–183 indications for, 175–178 motor area, 175–176 sensory area, 176 locations for, 175–178, 175f. See also under Cerebral cortex. motor area, 175, 175f sensory area, 175f, 176 for multiple sclerosis, 183–184 case reports on, 184–185 needle techniques for, 179 for phantom limb pain, 179–180 case report on, 180 for residual limb pain, 179–180 case report on, 180 for restless legs syndrome, 183 case report on, 183 for stroke, 180–181 case report on, 181–182 timing and frequency of, 179 interaction of, with fascia and loose connective tissue, 144, 145f medical, 139 adverse effects of, 148 clinical research on, 149–152 challenges of, 149–150 with elbow pain, 151 with fibromyalgia, 151 with headache, 150 with hip pain, 151 with knee pain, 150–151

Acupuncture (Continued) with postoperative pain, 151–152 with shoulder pain, 151 with spine pain, 150 with temporomandibular joint pain, 151 in complex chronic pain treatment, 142 conventional pain medicine integrated with, 152 cost effectiveness of, 148–149 as diversified therapy, 140 education for, 141 effects of, 141–142 on brain, 145–147 brain imaging of, 145, 146f history of, 139–140 mechanisms of, 143–147 twentieth century, 143, 144f twenty-first century, 143–144 more than needling, 141 neuromatrix theory of pain and, 142–143, 143f neuronal plasticity and, 146–147 for pain, optimal, 147–149 as mind-body treatment, 148 neuromusculoskeletal diagnosis in, 147–148 safety of, 148 systems theory and, 141–142 techniques of, 140–152 trigger point milieu and, 144 as unification of classical acupuncture and modern medicine, 140–141 in procedural pain management, 25 Acupuncture mode TENS, 561, 562t Acupuncture theory, of pain control, 561 Adjustive distraction, 567 Advanced Cardiac Life Support (ACLS) Protocol, 49 Alexander technique, 216–217, 218t–219t Alfentanil, for analgesia, 27 Allergic reactions to contrast agents, premedication for, 10 to spinal injections, 41 Allergies, 24–25 Alpha lipoic acid, in pain management, 188t–191t, 197 American Heart Association, Advanced Cardiac Life Support Protocol of, 49 Analgesics herbal centrally-acting, 188t–191t, 194–195 hypnotic, 188t–191t, 197 salicylate-containing, 188t–191t, 196–197 topical, 188t–191t, 195–196 hormonal, 188t–191t, 198–199

Page references followed by f indicate figure, by b indicate box, and by t indicate table. 619

620  Index

Anaphylactic reactions, to spinal injections, 41 Anaphylactoid reactions, to spinal injections, 41 Anesthesia, local. See Local anesthetics. Anesthetic blocks, 240 Anesthetic discography, discogenic pain or IDD diagnosis using, 448 Angelica sinensis (Dang Gui, Tang Kui, Dong Kuai), for inflammation, 188t–191t, 192–193 Anger, Hans Eysenck’s work on, 224 Ankle dysfunction, manual therapy for, outcomes research on, 588 Ankle mortise, corticosteroid injections in, 72–73, 73f–74f Ankylosing spondylitis, Tai Chi Chuan for, 216 Annuloplasty, 462 intradiscal electrothermal, 462 laser, percutaneous endoscopic, for radicular pain, 470 Anserine bursitis, injections for, 79–80, 79f Anterior ramus block, complications of, 44 Antiemetics, for sedation/analgesia, 25–26, 26t Antiinflammatory herbal medicines, 187–194, 188t–191t Appointment scheduling, 53 Aristocort. See Triamcinolone (Aristocort, Kenalog). Aristospan. See Triamcinolone hexacetonide (Aristospan). Arnica (Arnica montana), for topical analgesia, 188t–191t, 196 Arnica montana (Arnica), for topical analgesia, 188t–191t, 196 Arthritis. See Osteoarthritis (OA), Rheumatoid arthritis (RA). Arthrodesis, sacroiliac joint, efficacy of, 397 Asana (posture), in yoga, 205, 206f Ativan (lorazepam), in conscious sedation, 26 Atlantoaxial joint lateral, intraarticular blocks of interpretation of results of, 377 procedure for, 377, 378f–379f validity of, 377–378 pain map of, 363f Atlantooccipital joints intraarticular blocks of, 378–379, 379f pain map of, 363f Atlas, release of, 170, 170f Australian approach, to manual therapy, 576, 576f Automated percutaneous lumbar discectomy, 470–471 Axillary nerve block, ultrasound-guided, 248–249, 249f B Back pain chronic Alexander technique for, 217, 218t–219t massage therapy for, 211, 211t yoga for, benefits of, 206, 208f low. See Low back pain (LBP). percutaneous neuromodulation therapy for, 135–136 Pilates for, 209 Symphytum officinale for, 188t–191t, 196 BAI (Beck Anxiety Inventory), 17 Balloon microcompression, for trigeminal neuralgia, 302, 302f Barrier concept, in osteopathic manipulative medicine, 158, 159f BDI (Beck Depression Inventory), 17 Beck Anxiety Inventory (BAI), 17 Beck Depression Inventory (BDI), 17 Benzodiazepines, in conscious sedation, 26 Betamethasone acetate (Celestone Soluspan), 8 Betamethasone (Celestone), 7t, 8 adverse reactions to, 41 Betamethasone sodium phosphate, 8 Biacuplasty, intradiscal, for discogenic pain, 462, 463f efficacy of, 465 Biceps brachii tendinitis, corticosteroid injections for, 86, 86f Biopsychosocial model of pain, 14 Black Haw (Viburnum prunifolium), for painful conditions, 188t–191t, 200

Bleeding complicating selective spinal injections, 39, 41–42, 42f epidural steroid injection-related, 318 reduction of, cold therapy for, 555 Body awareness therapy (BAT), 217–219 Body work and movement therapies, 205 Alexander technique as, 216–217, 218t–219t body awareness therapy as, 217–219 massage as, 209–212, 211t. See also Massage therapy. mind body therapies as, 223 Pilates as, 208–209, 209t Tai Chi Chuan as, 213–216, 213f, 214t–215t yoga as, 205–208. See also Yoga. Bone pain, percutaneous neuromodulation therapy for, 136–137 Boswellia serrata (Frankincense), for inflammation, 188t–191t, 193 Botulinum toxin clinical use of, 97–99 history of, 97 injections of, in myofascial pain disorders, 97 cervical dystonia as, 99–100 myofascial pain syndrome as, 100–103 piriformis syndrome as, 103–106, 105f–106f Bradycardia, hypotension with, from spinal injections, treatment of, 51 Brain acupuncture effects on, 145–147 brain imaging of, 145, 146f infarct of, epidural steroid injection-related, 319 Brazilian Arnica (Solidago chilensis), for painful conditions, 188t–191t, 200 Bridging exercises for back pain, 605, 605f lumbar active range of motion, with static knee extension, for back pain, 605, 605f bilateral, on ball, for back pain, 605, 605f resist, for back pain, 605, 605f Bromelain, for inflammation, 188t–191t, 192 Bronchospasm from medications, treatment, 11 from spinal injections, treatment of, 51 Bruising, Arnica montana for, 188t–191t, 196 Bryonia alba (White Bryony), for analgesia, 188t–191t, 195 Bupivacaine (Marcaine), 6 adverse reactions to, 41 in procedural pain management, 28 for procedure, 3–4 uses of, 6t Burn injury, massage therapy for, 212 Burning mouth syndrome, Hypericum perforatum for, 188t–191t, 195 Bursae, anatomy of, 77 Bursae injections, 77 for bursitis. See Bursitis entries. pharmacologic agents for, 80–81, 81t role of, 77 Bursitis Achilles, injections for, 80 anserine, injections for, 79–80, 79f calcaneal, injections for, 80 iliopectineal, injections for, 79 infrapatellar, injections for, 80 ischial, injections for, 79 olecranon, injections for, 78, 78f overview of, 77 prepatellar, injections for, 80 retrocalcaneal (subtendinous), injections for, 80 subacromial (subdeltoid), injections for, 77–78, 78f subcutaneous, injections for, 80 tibial collateral ligament, injections for, 80, 80f trochanteric, injections for, 78–79, 79f Burst mode TENS, 561, 562t

Index  621

C Calcaneal bursitis, injections for, 80 California Poppy (Eschscholtzia californica), for hypnotic analgesia, 188t–191t, 197 CAM therapy. See Complementary and alternative medical (CAM) procedures. Canadian approach, to manual therapy, 577 Cancer pain massage therapy for, 212 neurolytic blocks for, 241 yoga for, benefits of, 208 Cannabis sativa (marijuana), for analgesia, 188t–191t, 194–195 Capsicum frutescens (Cayenne), for topical analgesia, 188t–191t, 195 Cardiopulmonary arrest, from medications, treatment of, 11 Cardiovascular complications, of selective spinal injections, 39–40 Carpal tunnel syndrome, yoga for, benefits of, 207 Carpometacarpal joint, corticosteroid injections in, 69, 69f Catastrophizing, patient, cognitive-behavioral therapy for, 20 Caudal epidural injections, complications of, 42 Caudal needle placement, for epidural steroid injections, 322–323, 323f–325f CBT (cognitive-behavioral therapy), in pain management, 20–21 Celestone. See Betamethasone (Celestone). Celestone Soluspan. See Betamethasone acetate (Celestone Soluspan). Celiac ganglia, anatomy of, 515 Celiac plexus block, 514–516 Celiac plexus, anatomy of, 514–515 Centella asiatica (Gotu Kola), for painful conditions, 188t–191t, 200 Cerebral cortex areas of, 174f balance area of, acupuncture of, 177, 177f foot motor and sensory area of, acupuncture of, 177–178, 178f gallbladder area of, acupuncture of, 178, 178f head area of, acupuncture of, 178, 178f internal organ areas of, acupuncture of, 178 large intestine area of, acupuncture of, 178, 178f liver area of, acupuncture of, 178, 178f motor area of, acupuncture of indications for, 175–176 location of, 175, 175f praxis area of, acupuncture of, 175f, 177 reproductive area of, acupuncture of, 178, 178f sensory area of, acupuncture of indications for, 176 location of, 175f, 176 speech I area of, acupuncture of, 175f, 177 speech II area of, acupuncture of, 175f, 177, 177f speech III area of, acupuncture of, 175f, 177 stomach area of, acupuncture of, 178, 178f thoracic cavity area of, acupuncture of, 178, 178f tremor and chorea area of, acupuncture of, 175f, 176–177 vascular dilation and constriction area of, acupuncture of, 175f, 177 vertigo and hearing area of, acupuncture of, 175f, 177 vision area of, acupuncture of, 177, 177f Cervical artery dysfunction, cervical manipulation and, 590–592, 591t Cervical discitis, complicating selective spinal injections, 39, 44 Cervical dystonia, botulinum toxin injections for, 99–100, 100t Cervical interlaminar epidural steroid injections, 328–333, 332f–338f Cervical spine discography of, 433–437. See also Discography, cervical. distraction of, positional, 569, 570f epidural injections in, complications of, 42, 44f loading of dynamic, 360 static, 360 manipulation of, adverse events associated with, 590–591 radicular pain from, 444, 447f strain counterstrain treatment of, 161–163, 163f traction on manual

Cervical spine (Continued) following inhibitive distraction, 568, 568f–569f in sitting position, 569, 569f mechanical (Saunders), 570–571, 571f over-the-door, 569–570, 570f techniques for, 568–571 transforaminal injections of, complications of, 8 zygapophysial joints of facets of, 358, 359f interventions for. See under Zygapophysial joint injections. pain map of, 363f, 444f pathology of, 361, 361f radiofrequency neurotomy of development of, 381 effectiveness of, 382–383 procedure for, 381–382, 382f Cervical transforaminal epidural steroid injections, 344–348, 347f–350f Cervicogenic dizziness, manual therapy for, outcomes research on, 586 Cervicogenic headache, diagnosis of, 362–363, 363f Check-in procedures, 53–54 Check-out procedures, 55 Chemical cold packs, 557 Chemical intradiscal therapies for discogenic pain, 467–468 for radicular pain, 469–470 Chemonucleolysis, 461 for radicular pain, 469–470 Chest wall surgery on, intercostal nerve block for, 289 trauma to, intercostal nerve block for, 289 Cheyenne (Capsicum frutescens), for topical analgesia, 188t–191t, 195 China, in history of acupuncture, 139–140 Chinese scalp acupuncture, 173. See also Acupuncture, Chinese scalp. 2-Chloroprocaine in procedural pain management, 28 uses of, 6t Chondroitin sulfate, in pain management, 188t–191t, 198 Chondromalacia patellae, 609 Chronic fatigue syndrome, coenzyme Q10 for, 188t–191t, 199 Chymopapain, for radicular pain, 469–470 Claim production, 55–56, 56t Claudication, intermittent, ginkgo for, 188t–191t, 200 Clinical prediction rules, in treatment-based classification, 584–585, 584f–585f, 585t Coccygodynia, refractory, prolotherapy for, 125 Coenzyme Q10 (CoQ10), in pain management, 188t–191t, 199 Cognitive behavioral therapy (CBT) in pain management, 20–21 in procedural pain management, 25 Cold packs, chemical, 557 Cold therapy, 555 application of, 556–558 biophysics of, 555 bleeding reduction from, 555 chemical cold packs in, 557 Cryocuff in, 557–558, 558f effects of, 555–556 gel packs in, 557, 557f ice baths in, 556, 556f ice massage in, 556–557, 557f ice packs/bags in, 556 indications for, 556 metabolic rate slowing from, 555 muscle spasm reduction from, 555 pain relief from, 555 precautions and contraindications for, 556 research studies on, 556 swelling reduction from, 555 vapocoolant sprays in, 558

622  Index

Colitis, collagenous, Boswellia serrata for, 188t–191t, 193 Collagenase, intradiscal, for radicular pain, 469 Collagenous colitis, Boswellia serrata for, 188t–191t, 193 Comfrey (Symphytum officinale), for topical analgesia, 188t–191t, 196 Complementary and alternative medical (CAM) procedures body work and movement therapies. See also Body work and movement therapies. body work and movement therapies as, 205 Chinese scalp acupuncture as, 173. See also Acupuncture, Chinese scalp. herbal and nutritional supplements in, 187. See also Herbal medicine; Herbal medicines. medical acupuncture as, 139. See also Acupuncture, medical. osteopathic manipulative medicine as, 155. See also Osteopathic manipulative medicine. percutaneous neuromodulation therapy as, 131. See also Percutaneous neuromodulation therapy (PNT). prolotherapy as, 113. See also Prolotherapy. Complex regional pain syndrome (CRPS) Chinese scalp acupuncture for, 179–180 case report on, 180 dimethyl sulfoxide for, 188t–191t, 196 Computed tomography, for chronic spinal pain, 527–530, 529f Connective tissue, loose, fascia and, interaction of acupuncture with, 144, 145f Connective tissue massage, 579 Conray (iothalamate), 10 Conscious sedation. See also Sedation/analgesia. definition of, 23 for interventional pain procedures, 23 Consent, informed, 57. See also Informed consent. “Consent to treatment” form, 58, 59f Contrast agents, 10 adverse reactions to, prophylaxis for, 51–52 allergic reactions to, premedication for, 10 in diagnostic sacroiliac joint injections, 395–396 in discography, 420 in epidural injections, medical issues related to, 316 in epidural steroid injections, 321 Conventional mode TENS, 561, 562t Convulsions, toxic, treatment of, 11 Coping skills development (CSD), in pain management, 20–21 Corticosteroid injections, 7–9 adverse reactions to, 9 bursae, 77. See also Bursae injections; Bursitis. drug interactions with, 9 epidural, 317 history of, 313 intraarticular in lower extremity, 71. See also Intraarticular injections, of corticosteroids, in lower extremity. in upper extremity, 63. See also Intraarticular injections, of corticosteroids, in upper extremity. mechanism of action of, 7–8 neurotoxicity of, 239, 239f spinal, 8–9 tendons/tendon sheaths, 83–88. See also Tendons/tendon sheaths, corticosteroid injections of. trigger point, 91 Corticosteroids, in epidural steroid injections, 321 Cortisone, 7t Corydalis yanhusuo (Yanhusuo), for analgesia, 188t–191t, 194 Cramp Bark (Viburnum opulus), for painful conditions, 188t–191t, 200 Cranial field, osteopathy in, 168–169 palpation exercise for, 169–170, 170f release of cranial base and atlas as, 170, 170f CRPS. See Complex regional pain syndrome (CRPS). Cryocuff, in cold therapy, 557–558, 558f

Cryotherapy, 555. See also Cold therapy. for trigeminal neuralgia, 301 CSD (coping skills development), in pain management, 20–21 CT myelography, for chronic spinal pain, 530, 530f Curcuma longa (Turmeric), for inflammation, 187–192, 188t–191t Current procedural terminology (CPT) codes, 54, 55t D Dang Gui (Angelica sinensis), for inflammation, 188t–191t, 192–193 Darana (concentration), in yoga, 205 De Quervain syndrome, corticosteroid injections for, 85, 85f Débridement, sacroiliac joint, efficacy of, 397 Decadron. See Dexamethasone (Decadron). Decompressive procedures, for trigeminal neuralgia, 302–303, 303f Degenerative disc disease, leg pain from, prolotherapy for, 125 Dehiscence, wound complicating implanted intrathecal drug infusion pumps, 499 complicating spinal cord stimulation, 493, 494f Depigmentation, complicating intraarticular upper extremity injections, 64 Depo-Medrol. See Methylprednisolone (Medrol, Depo-Medrol). Depression, Hans Eysenck’s work on, 224 Devil’s Claw (Harpagophytum procumbens), for inflammation, 188t–191t, 193 Dexamethasone acetate (Decadron-LA), 8 Dexamethasone (Decadron), 7t, 8 Dexamethasone sodium phosphate (Decadron Phosphate), 8 Dhyana (meditation), in yoga, 205 Diabetic neuropathic pain lipoic acid for, 188t–191t, 197 percutaneous neuromodulation therapy for, 136 vitamin D for, 188t–191t, 199 Diatrizoate (Renografin), 10 Diazepam (Valium), in conscious sedation, 26 Dimethyl sulfoxide (DMSO), for topical analgesia, 188t–191t, 196 Disc anatomy of, 409 compression fracture of, magnetic resonance imaging for, 537 degeneration of, 409–410 discogenic pain and, 444–447 disruption of, internal. See Internal disc disruption (IDD). morphology of, 409–411, 413 prolapse of, contained, radicular pain due to, 451–452 diagnosis of, 450 puncture of, safety of, 475 Disc biacuplasty, for discogenic pain, 462, 463f efficacy of, 465 Disc decompression, percutaneous, for radicular pain, 470–471 Disc herniation magnetic resonance imaging for, 532–533, 533f–538f nomenclature for, 532–533, 532f posterolateral, from lumbar epidural injection, 42, 43f Disc manometry, 413 Discectomy, lumbar, percutaneous, automated, 470–471 Discitis cervical, complicating selective spinal injections, 39, 44 complicating discography, 44, 414 Discogenic pain (DP), 441 criteria for, 421 definition of, 444 diagnosis of using anesthetic discography, 448 using specific nerve blocks, 447–448, 448f disc degeneration and, 444–447 internal disc disruption and, 447 intradiscal therapies for, 450–451 chemical, 467–468 thermal, 462–466 neural radiofrequency thermocoagulation for, 466–467 regenerative therapies for, 468–469

Index  623

Discography, 407 anesthetic, discogenic pain or IDD diagnosis using, 448 cervical, 413–414, 433–437 contraindications to, 419 equipment and supplies for, 433 pain maps from, 443–444, 445f–446f procedure for, 433–437, 435f–437f clinical application of, 411–412 complications of, 44–45, 45f, 414, 419 contraindications to, 419 as criterion standard test, 408–409 drapes for, 421 equipment for, 419 fundamental concepts of, 407, 408t history and development of, 407–408 internal disc disruption diagnosis with, 448–449, 449t, 450f interpretation of, 413 intravenous access for, 420 lumbar, 421–427 lateral or extrapedicular approach to, 421, 421f patient positioning for, 421 postprocedure care for, 421f, 427, 431f procedure note for, 438–439 single-needle technique for, 423 two-needle technique for, 423–424, 424f–431f medications for, 420 other tests compared with, 412 overview of, 407 pain and, 410–411 preparation for, 421 provocation. See Provocation discography (PD). provocation/analgesia assessment in, 413 sedation for, 420–421 supplies for, 419–420 technical performance of, 412–414 techniques of, 421 thoracic, 414, 427–432 equipment and supplies for, 430 procedure for, 430–432, 432f–434f training for, 419 Disease definition of, 14 illness differentiated from, 14 Distraction. See also Traction. adjustive, 567 definition of, 567 graded, 567 inhibitive, 567 cervical, 568, 568f positional cervical, 569, 570f lumbar, 571, 571f in procedural pain management, 25 rhythmic, 567 types of, 567 Dizziness cervicogenic, manual therapy for, outcomes research on, 586 in multiple sclerosis, Chinese scalp acupuncture for, case report on, 184–185 DMSO (Dimethyl sulfoxide), for topical analgesia, 188t–191t, 196 Dong Kuai (Angelica sinensis), for inflammation, 188t–191t, 192–193 Double crush syndrome, 239–240, 240f DP. See Discogenic pain (DP). Draftsmen’s elbow, injections for, 78, 78f Dural puncture complicating selective spinal injections, 40–41 epidural steroid injection-related, 318 Dutch approach, to manual therapy, 577

Dysmenorrhea Angelica sinensis for, 188t–191t, 192–193 Corydalis yanhusuo for, 188t–191t, 194 magnesium for, 188t–191t, 198 Viburnum for, 200 Zingiber officinalis for, 188t–191t, 193 Dysrhythmias complicating selective spinal injections, 40 from spinal injections, treatment of, 52 Dysthymia, electromagnetic. See Electromagnetic dysthymia (EMD). Dystonia, cervical, botulinum toxin injections for, 99–100, 100t E Echinacea spp. (Purple coneflower), for topical analgesia, 188t–191t, 196 Edema facial, from spinal injections, treatment of, 51 laryngeal, from spinal injections, treatment of, 51 pulmonary, from spinal injections, treatment of, 51 Effective dose equivalent, of radioactivity, annual individual, 33–34, 34t Elbow draftsmen’s, injections for, 78, 78f dysfunction of, manual therapy for, outcomes research on, 587–588 pain in acupuncture for, research on, 151 corticosteroid injections for, 67, 68f tennis corticosteroid injections for, 85–86, 85f prolotherapy for, 121–124 Elderly, musculoskeletal disorders in, Tai Chi Chuan for, 216 Electrical stimulation in pain control, 559 clinical acceptance of, on market, 565–566 efficacy of, evidence of, 564–565 historical perspective on, 559 interferential current, 563–564. See also Interferential current (IFC) stimulation. in modern medicine, 559–562 neuromuscular, 562–563. See also Neuromuscular electrical stimulation (NMES). safety precautions for, 564 transcutaneous electrical nerve stimulation in, 559 Electroacupuncture, percutaneous neuromodulation therapy differentiated from, 131 Electroconvulsive therapy, headache from, percutaneous neuromodulation therapy for, 137 Electromagnetic dysthymia (EMD). characteristics of, 224 mind body therapies for, 226 posttraumatic stress disorder and, 224–225 treatment protocol for, 226–227 Electromagnetic spectrum, 32f EMD. See Electromagnetic dysthymia (EMD). Endorphin hypothesis, of acupuncture analgesia, 143, 144f Endorphin theory, of pain control, 561, 561f Epicondylitis, lateral, corticosteroid injections for, 85–86, 85f Epicondylosis, lateral, prolotherapy for, 121–124 Epidural abscess complicating selective spinal injections, 39, 39f, 42f complicating spinal cord stimulation, 493–494 Epidural hematoma, complicating selective spinal injections, 40–42 Epidural injections, 313 care after, 348–350 caudal complications of, 42 needle placement for, 322–323, 323f–325f cervical complications of, 42, 44f interlaminar, 328–333, 332f–338f complications of, 317–319

624  Index

Epidural injections (Continued) contraindications for, 316 equipment for, 319–322 evaluation before, 315–316 history of, 313 indications for, 316 intravenous access for, 322 lumbar complications of, 42, 43f interlaminar, 323–325, 325f–329f sample dictation for, 351 medical issues related to, 316–317 negative predictors for, 316 periprocedure techniques for, 322–333 positive predictors for, 316 preparation and drapes for, 322 sedation for, 322 techniques of, 319–350 thoracic complications of, 43 interlaminar, 325–328, 329f–332f transforaminal technique for cervical, 344–348, 347f–350f sample dictation for, 351 lumbar, 335–344, 341f–343f S1, corticosteroid, 333–335, 338f–340f thoracic, 344, 344f–347f Epidural space, anatomy of, 314 Erector spinae assisted stretching, for back pain, 608, 608f Eschscholtzia californica (California Poppy), for hypnotic analgesia, 188t–191t, 197 Ethanol, intradiscal, for radicular pain, 469 Etidocaine, uses of, 6t Etomidate, for procedural sedation, 27 Exercise tolerance, omega-3 oils for, 188t–191t, 192 Exercises, therapeutic, 597. See also Therapeutic exercise(s). Extremity(ies) lower, myofascial release in, 168, 168f myofascial release in, 166–168 upper, myofascial release in, 167–168, 168f F FACES Pain Rating Scale, 16 Facet joint nerve blocks, complications of, 45 Facial edema, from spinal injections, treatment of, 51 Fake Bad Scale (FBS), 18 Family, in pain management, 21 Fascia description of, 144 loose connective tissue and, interaction of acupuncture with, 144, 145f Fasciitis, plantar corticosteroid injections for, 86, 86f prolotherapy for, 124 Fat necrosis, subcutaneous, complicating intraarticular upper extremity injections, 64 FBS (Fake Bad Scale), 18 Feldenkrais method, of body awareness therapy, 218 Femoral nerve block, ultrasound-guided, 250–251, 251f Fentanyl, for analgesia, 27 Feverfew (Tanacetum parthenium), for inflammation, 188t–191t, 194 Fibromyalgia acupuncture for, research on, 151 body awareness therapy for, 218–219 Chinese scalp acupuncture for, 182 case report on, 182–183 as contraindication to intradiscal therapies, 452 SAM-e for, 188t–191t, 198 yoga for, benefits of, 206 Film dosimetry system, for radiation exposure monitoring, 35–36

Flumazenil, as benzodiazepine antagonist, 26–27 Fluoroscopes, C-arm, 31–32, 33f Fluoroscopy, 31–32 epidural steroid injections guided by, 319–320 radiation exposure during factors affecting, 32–34 in selective spinal injections, 41 radiation risks during to patients, 34–35 to physician and assisting personnel, 35–36 sciatic nerve block guided by, 264–265, 265f suprascapular nerve block guided by, 258–259, 259f Foot, dysfunction of, manual therapy for, outcomes research on, 588 Fractures compression, osteoporotic, magnetic resonance imaging for, 537 insufficiency, magnetic resonance imaging for, 537, 544f Frankincense (Boswellia serrata), for inflammation, 188t–191t, 193 G Gamma rays, 32f definition of, 31 Ganglion(ia) celiac, anatomy of, 515 sphenopalatine anatomy of, 513 block of, 513–514. See also Sphenopalatine ganglion block. stellate anatomy of, 509 block of, 509–513. See also Stellate ganglion block. of Walther, block of, 517–518 Ganglion impar block, 517–518 Gasserian ganglion techniques, for trigeminal neuralgia, 301–302, 301f balloon microcompression as, 302, 302f glycerol injections as, 301–302 radiofrequency thermocoagulation as, 301, 301f Gate control theory of pain, 13 of pain control, 560, 560f Gel packs, in cold therapy, 557, 557f Genitofemoral nerve block, 281 anatomy relevant to, 281, 282f complications of, 283 contraindications for, 283 indications for, 281–282 technique for, 282–283, 282f Genitofemoral neuralgia etiology and pathogenesis of, 281 treatment options for, 283 Ginger (Zingiber officinalis), for inflammation, 188t–191t, 193 Ginkgo biloba (Ginkgo), for painful conditions, 199–200 Glenohumeral joint, corticosteroid injections in, 65–66, 65f–66f Glucosamine sulfate, in pain management, 188t–191t, 198 Glycerol injections, for trigeminal neuralgia, 301–302 Gotu Kola (Centella asiatica), for painful conditions, 188t–191t, 200 Graded distraction, 567 Granulomatous spondylitis, magnetic resonance imaging for, 526f–527f, 536–537 Granulomatous spondylodiscitis, magnetic resonance imaging for, 537, 543f Gray rami communicantes, radiofrequency of, for discogenic pain, 466–467 Grimsby approach, to manual therapy, 577 Group therapy, in pain management, 21 H HAMD (Hamilton Depression Rating Scale), 17 Hamilton Depression Rating Scale (HAMD), 17 Hamstring curls, for back pain, 604, 604f Hamstring stretching exercises, assisted, for back pain, 604, 604f Hand dysfunction, manual therapy for, outcomes research on, 588

Index  625

Harpagophytum procumbens (Devil’s Claw), for inflammation, 188t–191t, 193 Headache acupuncture for, research on, 150 cervicogenic, diagnosis of, 362–363, 363f manual therapy for, outcomes research on, 586–587 melatonin for, 188t–191t, 198 migraine. See Migraine. post-electroconvulsive therapy, percutaneous neuromodulation therapy for, 137 Heat modalities in pain management, 551. See also Thermal applications. Hematoma(s) complicating sciatic nerve block, 265 complicating selective spinal injections, 40–42, 42f complicating spinal cord stimulation, 493–494 epidural steroid injection-related, 318 Herbal medicine Chinese, 187–200 western, 187 Herbal medicines analgesic centrally-acting, 188t–191t, 194–195 hypnotic, 188t–191t, 197 salicylate-containing, 188t–191t, 196–197 topical, 188t–191t, 195–196 antiinflammatory, 187–194, 188t–191t Herniation, disc. See Disc herniation. Herpes zoster infection, pain from, percutaneous neuromodulation therapy for, 137 High velocity low amplitude technique, for thoracic spine, 163–164 in extended dysfunction, 165–166, 165f–166f in flexed dysfunction, 165, 165f Hip adductor tendinopathy, prolotherapy for, 124 Hip capsule, posterior, stretching of, for back pain, 606, 606f–607f Hip joint dysfunction of, manual therapy for, outcomes research on, 588 pain in acupuncture for, research on, 151 corticosteroid injections for, 71, 72f therapeutic exercises for, 613–614, 613f–614f proprioceptive exercises for, using trampoline, for hip pain, 613, 614f Hormonal analgesics coenzyme Q10 as, 188t–191t, 199 melatonin as, 188t–191t, 198 vitamin D as, 188t–191t, 198–199 Hot packs, 551, 552f Housemaid’s knee, injections for, 80 Huang qin (Scutellaria baicalensis), for painful conditions, 188t–191t, 200 Hyaluronic acid, for viscosupplementation, 10 Hydrocollator packs, 551, 552f Hydrocortisone (cortisol), 7t Hypercorticism, complicating intraarticular upper extremity injections, 64 Hypericum perforatum (St. John’s Wort), for analgesia, 188t–191t, 195 Hypertension, from spinal injections, treatment of, 51 Hypnosis, in procedural pain management, 25 Hypnotic analgesic herbs, 188t–191t, 197 Hypotension with bradycardia, from spinal injections, treatment of, 51 with tachycardia, from spinal injections, treatment of, 51 I ICD-9-CM codes, 54 Ice baths, 556, 556f Ice massage, 556–557, 557f Ice packs/bags, 556 IDD. See Internal disc disruption (IDD).

IDET. See Intradiscal electrothermal therapy (IDET). Iliohypogastric nerve block, 285 anatomy relevant to, 285, 286f complications of, 287 contraindications for, 287 indications for, 285–286 technique for, 286–287, 286f–287f Ilioinguinal nerve block, 285 anatomy relevant to, 285, 286f complications of, 287 contraindications for, 287 indications for, 285–286 technique for, 286–287, 286f–287f Iliopectineal bursitis, injections for, 79 Iliopsoas stretching self-, for back pain, 607, 607f in side-lying position, for back pain, 607, 607f in supine position, for back pain, 607, 607f Iliotibial band tendinitis, corticosteroid injections for, 86 Illness definition of, 14 disease differentiated from, 14 Implanted pulse generator (IPG) pockets for, pain in, complicating spinal cord stimulation, 494 in spinal cord stimulation, 483, 484f, 485 Infection(s) complicating implanted intrathecal drug infusion pumps, 499 complicating intraarticular upper extremity injections, 64 complicating sciatic nerve block, 265 complicating selective spinal injections, 38–39 complicating spinal cord stimulation, 493 epidural steroid injection-related, 317–318 Informed consent, 57 avoiding legal entanglements with, 58 documentation for, 58, 59f legal framework for, 57 patient’s role in, 58 physician’s role in, 57–58 Infraclavicular nerve block, ultrasound-guided, 247–248, 248f–249f Infrapatellar bursitis, injections for, 80 Inhibitive distraction, 567 cervical, 568, 568f Injections, intraarticular. See Intraarticular injections, of corticosteroids. Instantaneous axes of rotation (IARs), in spine, movement and, 359 Insurance verification, 53 Integrated Psychosocial-Spiritual Model, of pain management, 21 Intercarpal joints, corticosteroid injections in, 69 Intercostal nerve block, 289 complications of, 45, 292 indications for, 289 technique for, 289–292, 291f Intercostal nerves, anatomy of, 290f, 289 Intercostal neuralgia, pathophysiology of, 289 Interferential current (IFC) stimulation, in pain control, 563–564, 563f clinical use and application of, 564 efficacy of, evidence of, 565 electrode placement for, 564f, 561 practical application of, 564 proposed mechanisms of, 563–564 Wedensky inhibition and, 564 Intermittent claudication, ginkgo for, 188t–191t, 200 Internal disc disruption (IDD), 441 clinical tests predicting, 412 diagnosis of criteria for, 462t provocation discography in, 461 using anesthetic discography, 448 using discography, 448–449, 449t, 450f

626  Index

Internal disc disruption (Continued) diagnostic criteria for, 409t discogenic pain and, 447 intradiscal therapies for, 450–451 MRI in assessment of, 412 prediction of clinical tests in, 450 magnetic resonance imaging in, 450 Interphalangeal joints, corticosteroid injections in, 69 Interscalene nerve block, ultrasound-guided, 246, 247f Intertarsal joints, corticosteroid injections in, 74 Intervertebral disc. See Disc and Disc entries. Intraarticular injections, of corticosteroids in lower extremity, 71 in ankle mortise, 72–73, 73f–74f in hip, 71, 72f in intertarsal joints, 74 in knee, 71–72, 73f in metatarsophalangeal joints, 74, 74f in subtalar joint, 74 in upper extremity acromioclavicular joint, 66–67, 66f–67f actions of, 63 alternatives to corticosteroids for, 64 with anesthetic, 63 in carpometacarpal joint, 69, 69f contraindications and complications of, 64 dosages for, 63 drug selection for, 63 in elbow, 67, 68f glenohumeral joint, 65–66, 65f–66f indications for, 63 in intercarpal joints, 69 in interphalangeal joints, 69 in sternoclavicular joint, 67, 67f techniques for, 64–65 in wrist, 68, 68f–69f for zygapophysial joint pain, 380–381, 380f–381f Intradiscal biacuplasty, for discogenic pain, 462, 463f Intradiscal electrothermal annuloplasty, 462, 462f Intradiscal electrothermal therapy (IDET) for discogenic pain, 462, 462f efficacy of, 463–465, 464f prospective cohort study on, 464–465 randomized controlled studies on, 464 technical performance of, 472–473, 476f–477f Intradiscal therapies, 461 chemical for discogenic pain, 467–468 for radicular pain, 469–470 complications of, 473–475 contraindications for, 452–454 disc access for, 471 discogenic pain and, 450–451 electrothermal. See Intradiscal electrothermal therapy (IDET). identifying anatomy and marking entry point for, 471 for intradiscal disc disruption, 450–451 needle preparation for, 471 patient positioning for, 471 postprocedural management of, 473 preventing need for, 453–454 procedure for, 471–472, 472f–473f technical performance of, 471–475 thermal, for discogenic pain, 462–466 Intrathecal drug infusion pumps, implanted, 494–502 catheters for, 496, 496f failure of, 501–502, 501f inflammatory mass at tip of, 502 contraindications for, 495 drug trial for, 496–497, 497t

Intrathecal drug infusion pumps (Continued) implant process for, 497–499, 498f–499f indications for, 495 infusion system failure in, 500–502 managing patients with, 500 medications for, 495 patient selection for, 495 postoperative complications of, 499 preimplant considerations for, 496 refilling pump reservoir in, 499–500 complications of, 500 types of, 495, 495f–496f Intravascular injection, complicating sciatic nerve block, 265 Intravenous access, for discography, 420 Iodinated contrast agents, adverse reactions to, prophylaxis for, 51–52 Iodine, allergies to, 24 Ionizing radiation, definition of, 31 Iothalamate (Conray), 10 IPG. See Implanted pulse generator (IPG). Ischial bursitis, injections for, 79 J Jamaican Dogwood (Piscidia spp.), for hypnotic analgesia, 188t–191t, 197 Japan, in history of acupuncture, 140 Joint pain, Urtica dioica for, 188t–191t, 196 Joint play tests, in physical examination, 581 Joints, injections into. See Intraarticular injections, of corticosteroids. K Kaltenborn-Evjenth approach, to manual therapy, 576 Kenalog. See Triamcinolone acetonide (Kenalog). Ketamine, for procedural sedation, 27 Knee dysfunction of, manual therapy for, outcomes research on, 588 exercises for closed chain, for hip pain, 614, 614f proprioceptive, using trampoline, for hip pain, 613, 614f housemaid’s, injections for, 80 pain in acupuncture for, research on, 150–151 bromelain for, 192 corticosteroid injections for, 71–72, 73f prolotherapy injections for, 114, 115f therapeutic exercises for, 609–611, 611f–613f. See also Therapeutic exercise(s), for knee pain. Knee squats with dumbbell, for knee pain, 611, 612f isometric, for knee pain, 611, 612f resist, for knee pain, 611, 612f–613f Knee step up/down, lateral partial, active range of motion, for knee pain, 611, 611f Knee wall slide, bilateral, active range of motion, for knee pain, 611f, 611 L Labor pain acupuncture for, research on, 152 massage therapy for, 212 Laminotomy leads, permanent implantation of, for spinal cord stimulation, 490–491 Laryngeal edema, from spinal injections, treatment of, 51 Laser annuloplasty, percutaneous endoscopic, for radicular pain, 470 Lateral epicondylitis, corticosteroid injections for, 85–86, 85f Lateral epicondylosis, prolotherapy for, 121–124 Lateral femoral cutaneous nerve anatomy of, 271, 272f–274f compression of, 271–272. See also Meralgia paresthetica (MP).

Index  627

Lateral femoral cutaneous nerve block, 271 classic technique for, 276 complications of, 277–278 contraindications to, 277–278 for meralgia paresthetica, 274 with nerve stimulator, 276 ultrasound-guided, 276–277, 277f Latex allergies, 24 LBP. See Low back pain (LBP). Leads, in spinal cord stimulation dislodgement of, 494 laminotomy, permanent implantation of, 490–491, 491f paddle, 490–491 percutaneous placement of, 488–490, 488f–490f surgical implantation of, 490, 490f Leg pain from degenerative disc disease, prolotherapy for, 125 Levator scapulae stretching exercises, for neck pain, 600, 600f Lidocaine, 6 adverse reactions to, 41 allergies to, 28 in procedural pain management, 28 for procedure, 3–4 uses of, 6t Ligaments, injection of, in prolotherapy, 114 Linear array transducers, for nerve blocks, 244, 244f Lipoic acid, in pain management, 188t–191t, 197 Local anesthetics, 5–7 allergies to, 24–25 for bursal injections, 80–81, 81t categorization of, 235t classification and uses of, 6t in epidural injections, medical issues related to, 316–317 in epidural steroid injections, 321 maximum allowable dose of, 236, 236t mechanism of action of, 5 pharmacology of, for nerve blocks, 233–236, 235t for procedure, 3–4 sedation/analgesia and, 28 in spinal injections, complications of, 41 toxicity of, 6–7 in trigger point injections, 89 vasoconstrictors with, 235–236 contraindications to, 235–236, 236t Lorazepam (Ativan), in conscious sedation, 26 Low back pain (LBP) acute, therapeutic exercises for, evidence on use of, 603–604, 603t Alexander technique for, 217, 218t assessing patients with, red flags in, 602t body awareness therapy for, 219 chronic, therapeutic exercises for, evidence on use of, 603–604, 603t classification of, treatment-based, 583t differential diagnosis of, 523t Harpagophytum procumbens for, 188t–191t, 193 imaging modalities for, 525t massage therapy for, 211–212 mechanical, manual therapy for, outcomes research on, 587 nonspecific, 442 prevention of, 453–454 percutaneous neuromodulation therapy for, 135–136 Pilates for, 209 prolotherapy for, 124–125 Salix alba for, 188t–191t, 196 social and economic dimension of, 441 Solidago chilensis for, 188t–191t, 200 subacute, therapeutic exercises for, evidence on use of, 603–604, 603t therapeutic exercises for, 601–609. See also Therapeutic exercise(s), for low back pain. vitamin D for, 188t–191t, 199 yoga for, benefits of, 205–206, 207t

Lower extremity joint injections in, 71. See also Intraarticular injections, of corticosteroids, in lower extremity. nerve blocks in. See also specific types of nerve blocks, e.g. Saphenous nerve block. ultrasound-guided, 250–252 tendon/tendon sheath injections in, 86, 86f Lumbar disc, entry to, for interdiscal therapy, 471–472, 472f–473f Lumbar discectomy, percutaneous, automated, 470–471 Lumbar interlaminar epidural steroid injections, 323–325, 325f–329f sample dictation for, 351 Lumbar plexus block, parasacral approach to, 262–263 Lumbar spine bridging exercises for active range of motion, with static knee extension, for back pain, 605, 605f bilateral, on ball, for back pain, 605, 605f resist, for back pain, 605, 605f discography of, 421–427. See also Discography, lumbar. epidural injections in, complications of, 42, 43f extension of, prone high level, active range of motion, for back pain, 608, 609f loading of dynamic, 360 static, 360 manipulation of, adverse events associated with, 590 muscle energy treatment for, 158–161, 160f painful conditions of, imaging for, accuracy of, 524t positional distraction of, 571, 571f radicular pain from, 444 rotation of, with ball, active range of motion, for back pain, 606, 606f stabilization of, for back pain, 609, 609f stretch of, with rotation, for back pain, 608, 608f traction on mechanical (Saunders), 571–572, 571f techniques of, 571–572 transforaminal injections of, complications of, 8 zygapophysial joints of facets of, 358, 359f pain map of, 364f pathology of, 361, 362f radiofrequency neurotomy of effectiveness of, 383–385 procedure for, 383, 383f Lumbar sympathetic block, 509–513, 516f Lumbar transforaminal epidural steroid injections, 335–344, 341f–343f Lymphatic drainage, manual, 579 Lymphedema, manual therapy in, 588 M Magnesium, in pain management, 188t–191t, 198 Magnetic resonance imaging (MRI) for chronic spinal pain, 530–538 in degenerative disease, 531–536, 531f–541f in systemic disease, 536–538, 542f–544f in internal disc disruption prediction, 450 Maitland (Australian) approach, to manual therapy, 576, 576f Mandibular nerve, 297, 298f Mandibular nerve block, for trigeminal neuralgia, 300 Manipulation, adverse events associated with major, 590–592 minor, 589 Manipulative medicine, osteopathic, 155. See also Osteopathic manipulative medicine. Manometry, disc, 413 Manual lymphatic drainage, 579 Manual therapy, 573. See also Physical therapy. adverse events associated with major, 590–592 minor, 589–590

628  Index

Manual therapy (Continued) approaches to, 576–581 Canadian approach to, 577 contraindications for, 589, 589t diagnostic classification in, 582 clinical guideline indices in, 582–583 clinical prediction rules in, 584–585, 584f–585f, 585t mechanism-based, 582–583 mixed indices in, 582 prognostic indices in, 582 status indices in, 582 treatment-based, 582–583, 583t Dutch approach to, 577 in early medicine, 573–574 in examination, 581–582 Grimsby approach to, 577 history of, 573–575 indications for, 586 joint stabilization and, 579 Kaltenborn-Evjenth approach to, 576 in lymphedema, 588 Maitland (Australian) approach to, 576, 576f massage as, 578–579. See also Massage/massage therapy (MT). McKenzie approach to, 577 in mechanical diagnosis and therapy, 577 mechanical effects of, 579–580 mechanisms of action of, 579 Mulligan approach to, 577, 577f neural mobilization approaches to, 577, 578f neurophysiologic effects of, 580 outcomes research on, 586 Paris approach to, 576–577 psychological effects of, 580–581 risk of harm associated with, evidence on, 589 soft-tissue mobilization as, 578–579, 578f in systemic conditions, 588 Manual trigger point therapy, 578 Marcaine. See Bupivacaine (Marcaine). Marijuana (Cannabis sativa), for analgesia, 188t–191t, 194–195 Massage/massage therapy (MT), 578–579 acupressure, 579 connective tissue, 579 history of, 209–210 ice, 556–557, 557f for muscle recovery after intense exercise, 211–212 for pain burn, 212 cancer, 212 chronic back, 211, 211t in labor, 212 low back, 211–212 in newborn, 212 postoperative, 212 surveys of, 210 risk of harm associated with, evidence on, 589 stroke techniques for, 210 Materiality definition of, 58 informed consent and, 58 Maxillary nerve, 297, 298f Maxillary nerve block, for trigeminal neuralgia, 300, 300f MBMD (Millon Behavioral Medicine Diagnostic), 19–20 McGill Pain Questionnaire (MPQ), 16 McKenzie approach, to manual therapy, 577 MCMI-III (Millon Clinical Multiaxial Inventory– Third Edition), 19 Mechanical effects, of manual therapy, 579–580 Mechanotransduction, acupuncture analgesia and, 144

Medial branch nerve blocks, 366–376 cervical C7, procedure for, 371, 371f C3 to C6 interpretation of results of, 370–371 procedure for, 366–370, 367f–370f third occipital, procedure for, 371–372, 372f–373f validity of, 372–373 development of, 366 lumbar interpretation of results of, 376 procedure for, 375–376, 375f–376f validity of, 376 thoracic interpretation of results of, 374 procedure for, 374, 374f–375f validity of, 375 Medial branch nerve(s), radiofrequency neurotomy of cervical development of, 381 effectiveness of, 382–383 procedure for, 381–382, 382f lumbar effectiveness of, 383–385 procedure for, 383, 383f thoracic, 383 Median nerve block, ultrasound-guided, 249, 249f–250f Medical acupuncture, 139. See also Acupuncture, medical. Medical negligence, 59–60 Medications in discography, 420 in epidural steroid injections, 321–322 infusion pumps for, intrathecal, implanted, 494–502. See also Intrathecal drug infusion pumps, implanted. Medicolegal issues, 57 doctor-patient relationship and, 58–59 informed consent as, 57–58 medical negligence as, 59–60 Meditation, mindfulness, in pain management, 21 Medrol. See Methylprednisolone (Medrol, Depo-Medrol). Melatonin, for painful conditions, 188t–191t, 198 Meperidine, for postoperative pain, 27–28 Mepivacaine, uses of, 6t Meralgia paresthetica (MP) diagnosis of, 272–274, 275f–276f etiology of, 271–272, 274f pathophysiology of, 272, 275f treatment of, 274–275 Mesmerism, 225 Metabolic rate, slowing of, cold therapy for, 555 Metatarsophalangeal joints, corticosteroid injections in, 74, 74f Methylene blue, intradiscal, for discogenic pain, 468 Methylprednisolone (Medrol, Depo-Medrol), 7t, 8 adverse reactions to, 41 Methylsulfonylmethane (MSM), in pain management, 188t–191t, 197 Meyers Validity in Chronic Pain Index, 18 Microconvex transducers, for nerve blocks, 244–245, 245f Microvascular decompression, for trigeminal neuralgia, 302–303, 303f Mid-thigh sciatic nerve block, ultrasound-guided, 264 Midazolam (Versed), in conscious sedation, 26 Migraine coenzyme Q10 for, 188t–191t, 199 ginkgo for, 188t–191t, 199 melatonin for, 188t–191t, 198 pediatric, magnesium for, 188t–191t, 198 prophylaxis for, thioctic acid in, 188t–191t, 197 riboflavin for, 188t–191t, 197 Tanacetum parthenium for, 188t–191t, 194 vitamin D for, 188t–191t, 199

Index  629

Migraine (Continued) yoga for, benefits of, 207 Zingiber officinalis for, 188t–191t, 193 Millon Behavioral Medicine Diagnostic (MBMD), 19–20 Millon Clinical Multiaxial Inventory–Third Edition (MCMI-III), 19 Mind body therapies, 223 clinical applications of, 226 definition of, 225 for electromagnetic dysthymia, 226 protocol for, 226–227 history and overview of, 225 interface of, with other complementary and alternative modalities, 227 for posttraumatic stress disorder, protocol for, 226–227 posttraumatic stress disorder and, 225–226 research summary and conclusion on, 227 Mindfulness meditation, in pain management, 21 Minnesota Multiphasic Personality Inventory–Second Edition (MMPI-2), 17–19 Restructured Form, 19 MMPI-2 (Minnesota Multiphasic Personality Inventory–Second Edition), 17–19 Restructured Form, 19 Modulated mode TENS, 562, 562t Monitoring, during selective spinal injections, 38 Morphine, for postoperative pain, 27–28 Motion palpation tests, in physical examination, 581, 581t Motion stacking, in myofascial technique, 166–167 Motor area of cerebral cortex, acupuncture of indications for, 175–176 location of, 175, 175f Motor blocks, 240 MP. See Meralgia paresthetica (MP). MPQ (McGill Pain Questionnaire), 16 MSM (methylsulfonylmethane), in pain management, 188t–191t, 197 MT. See Massage/massage therapy (MT). Mulligan approach, to manual therapy, 577, 577f Multiple sclerosis Chinese scalp acupuncture for, 183–184 vitamin D for, 188t–191t, 199 Muscle energy treatment, lumbar, 158–161, 160f Muscle spasm, reduction of, cold therapy for, 555 Musculoskeletal pain, management of, prolotherapy in, 113. See also Prolotherapy. Myalgia, statin-related, vitamin D for, 188t–191t, 199 Myofascial pain disorders, botulinum toxin injections in, 97. See also Botulinum toxin, injections of, in myofascial pain disorders. Myofascial pain syndrome, botulinum toxin injections for, 100–103 Myofascial release, in extremities, 166–168 lower, 168, 168f palpation exercise for, 167 upper, 167–168, 168f N Naloxone, for opioid reversal, 28 Neck pain acute, therapeutic exercises for, evidence on use of, 598–599, 598t chronic, therapeutic exercises for, evidence on use of, 599, 599t classification of, treatment-based, 583t mechanical, manual therapy for, outcomes research on, 586 therapeutic exercises for. See also Therapeutic exercise(s), for neck pain. Needle insertion, for procedure, 3–4 Needling trigger point injections with, physical findings before, during and after, 89, 93f, 93t for trigger points and tender spots, 89

Negligence, medical, 59–60 Neoplasms, spinal, magnetic resonance imaging for, 537–538 Nerve(s) genitofemoral, anatomy of, 281, 282f iliohypogastric, anatomy of, 285, 286f ilioinguinal, anatomy of, 285, 286f injury to, in nerve blocks, 238–240, 239f–240f intercostal, anatomy of, 289, 290f lateral femoral cutaneous anatomy of, 271, 272f–274f compression of, 271–272. See also Meralgia paresthetica (MP). occipital, anatomy of, 305, 306f saphenous anatomy of, 267, 268f entrapment of, pathophysiology and symptoms of, 267–268 sciatic, anatomy of, 261, 262f supraorbital, anatomy of, 293, 294f–295f suprascapular, anatomy of, 255, 256f trigeminal, anatomy of, 297, 298f Nerve blocks. See also specific types of nerve blocks, e.g. Suprascapular nerve block. basic principles of, 233 contraindications for, 233, 234t in discogenic pain diagnosis, 461 discogenic pain diagnosis using, 447–448, 448f education, training, and simulation for, 241 facet joint, complications of, 45 general principles of, 240–241 anesthetic blocks, 240 motor blocks, 240 neurolytic blocks, 241 sensory blocks, 240–241 genitofemoral, 281. See also Genitofemoral nerve block. iliohypogastric, 285. See also Iliohypogastric nerve block. ilioinguinal, 285. See also Ilioinguinal nerve block. indications for, 233, 234t intercostal, 289. See also Intercostal nerve block. lateral femoral cutaneous, 271. See also Lateral femoral cutaneous nerve block. local anesthetic pharmacology and, 233–236, 235t. See also Local anesthetics. medial branch, 366–376. See also Medial branch nerve blocks. nerve injuries during, 238–240, 239f–240f neurovascular bundle anatomy and, 233 occipital complications of, 307–308 indications for, 306–307, 307f–308f saphenous, 267. See also Saphenous nerve block. sciatic, 261. See also Sciatic nerve block. selective spinal, transforaminal injections versus, 333 sphenopalatine ganglion, 513–514. See also Sphenopalatine ganglion block. splanchnic, 514–515 stellate ganglion, 509–513. See also Stellate ganglion block. supraorbital, 293. See also Supraorbital nerve block. suprascapular, 255. See also Suprascapular nerve block. sympathetic, 507. See also Sympathetic neural blockade. complications of, 45 techniques of, 237–238, 237f–239f ultrasound-guided, 243. See also Ultrasound-guided nerve blocks. Nerve fibers, classification of, 236t Nerve root blocks, complications of, 44 Nerve stimulator, lateral femoral cutaneous nerve block with, 276 Neural mobilization approaches, to manual therapy, 577, 578f Neuralgia genitofemoral, etiology and pathogenesis of, 281 iliohypogastric etiology and pathogenesis of, 285 treatment options for, 287–288

630  Index

Neuralgia (Continued) ilioinguinal etiology and pathogenesis of, 285 treatment options for, 287–288 intercostal, pathophysiology of, 289 occipital, 305. See also Occipital neuralgia. supraorbital other treatments for, 295 pathophysiology of, 293 trigeminal, head and facial, 297. See also Trigeminal neuralgia. Neurectomy, for trigeminal neuralgia, 300–301 Neurologic complications, of selective spinal injections, 40 Neurolytic agents, 9 phenol as, 9–10 Neurolytic blocks, 241 for cancer pain, 241 for spasticity, 241 for trigeminal neuralgia, 301 Neuromatrix theory of pain, 13–14, 142–143, 143f Neuromodulation therapy, percutaneous, 131. See also Percutaneous neuromodulation therapy (PNT). Neuromuscular electrical stimulation (NMES), 562–563 in pain control, 562–563 clinical use and application of, 563 efficacy of, evidence of, 565 electrode placement for, 563 practical application of, 563 proposed mechanisms of, 563 Neuromusculoskeletal diagnosis, in optimal acupuncture pain therapy, 147–148 Neuronal plasticity, medical acupuncture and, 146–147 Neuropathic pain botulinum toxin for, 98–99 Cannabis sativa for, 188t–191t, 194 diabetic. See Diabetic neuropathic pain. local, as contraindication to intradiscal therapies, 452 percutaneous neuromodulation therapy for, 136 Neuropathy genitofemoral etiology and pathogenesis of, 281 genitofemoral nerve block for, 281–282, 282f treatment options for, 283 Hypericum perforatum for, 188t–191t, 195 Neurophysiologic effects, of manual therapy, 580 Neurostimulation, for trigeminal neuralgia, 303 Neurotomy, radiofrequency for sacroiliac joint pain cooled, 399–400, 401f efficacy of, 396–397 methods of, 399 traditional, 399, 399–400, 400f pulsed, 399 simplicity, 399–400, 401f–402f for zygapophysial joint pain cervical development of, 381 effectiveness of, 382–383 procedure for, 381–382, 382f lumbar effectiveness of, 383–385 procedure for, 383, 383f thoracic, 383 Neurotoxicity, in nerve blocks, 239, 239f Neurovascular bundle anatomy, 233, 235f Newborn, pain in, massage therapy for, 212 Niyama (personal behavior), in yoga, 205 Nociception, 360 in biopsychosocial model of pain, 14 Nociceptors, 131

Nonspecific low back pain (NSLBP), 442 prevention of, 453–454 Nonspecific spinal pain (NSSP), 442–444 reality of, 452–453 Nuclear medicine imaging, for chronic spinal pain, 538, 544f Nucleoplasty for radicular pain, 470 technical performance of, 472, 473f–476f Nutritional cofactors, 197–198 alpha lipoic acid as, 197 chondroitin sulfate as, 188t–191t, 198 glucosamine sulfate as, 188t–191t, 198 lipoic acid as, 188t–191t, 197 magnesium as, 188t–191t, 198 methylsulfonylmethane as, 197 riboflavin as, 188t–191t, 197 S-adenosyl methionine as, 188t–191t, 197–198 thioctic acid as, 188t–191t, 197 O OA. See Osteoarthritis (OA). Objective personality tests, in psychological pain evaluation, 15, 17 Occipital nerve anatomy, 305, 306f Occipital nerve block complications of, 307–308 indications for, 306–307, 307f–308f Occipital neuralgia, 305 continuous acute, 305 chronic, 305 diagnosis of, 306 paroxysmal, 305 symptoms of, 305–306 ODQ (Oswestry Low Back Pain Disability Questionnaire), 16–17 Olecranon bursitis, injections for, 78, 78f Omega-3 oils, for inflammation, 188t–191t, 192 Ophthalmic nerve, 297, 298f Ophthalmic nerve block, for trigeminal neuralgia, 299–300, 300f Opiate-mediated theory, of pain control, 561, 561f Opioid analgesics, 27–28 Osteoarthritis (OA) Arnica montana for, 188t–191t, 196 Boswellia serrata for, 188t–191t, 193 bromelain for, 188t–191t, 192 chondroitin sulfate for, 188t–191t, 198 Curcuma longa for, 187, 188t–191t glucosamine sulfate for, 188t–191t, 198 of hip, Tai Chi Chuan for, 215 of knee Tai Chi Chuan for, 215 therapeutic exercises for, 609–610 yoga for, benefits of, 206 methylsulfonylmethane for, 188t–191t, 197 omega-3 oils for, 188t–191t, 192 prolotherapy for, 125–126 Rosa canina for, 200 Salix alba for, 188t–191t, 196 SAM-e for, 188t–191t, 198 Scutellaria for, 188t–191t, 200 Symphytum officinale for, 188t–191t, 196 Tai Chi Chuan for, 215–216 yoga for, benefits of, 207–208 Zingiber officinalis for, 188t–191t, 193 zygapophysial joint, magnetic resonance imaging for, 535–536, 540f–541f Osteomalacia, vitamin D for, 188t–191t, 199 Osteomyelitis, vertebral, complicating selective spinal injections, 39f Osteopathic manipulative medicine, 155 history of, 155–156

Index  631

principles of, 156–158 diagnostic, 156–158, 158f treatment in, 158–164 Osteopathic manipulative medicine (Continued) barrier concept in, 158, 159f in cranial field, 168–169 palpation exercise for, 169–170, 170f release of cranial base and atlas as, 170, 170f direct, 158 high velocity low amplitude, thoracic spine, 163–164 indirect, 158 muscle energy, lumbar, 158–161, 160f myofascial release in extremities, 166–168, 168f palpation exercise for, 167 strain counterstrain, cervical region, 161–163, 163f Osteoporotic compression fractures, magnetic resonance imaging for, 537 Oswestry Low Back Pain Disability Questionnaire (ODQ), 16–17 Otitis media, Hypericum perforatum for, 188t–191t, 195 Ozone, intradiscal, for radicular pain, 470 P Paddle leads, for spinal cord stimulation, 490–491 PAI (Personality Assessment Inventory), 19 Pain. See also specific joint, e.g. Knee pain. from acute herpes zoster infection, percutaneous neuromodulation therapy for, 137 biopsychosocial model of, 14 cognitive-behavioral therapy for, 20–21 coping skills development for, 20–21 definition of, 360 discogenic, 441. See also Discogenic pain (DP). gate control theory of, 13 implanted intrathecal drug infusion pumps for, 495 management of family considerations for, 21 Integrated Psychosocial-Spiritual Model in, 21 mindfulness meditation in, 21 modes of therapy in, 21 as mind-body problem, acupuncture and, 148 models of, 13–14 neuromatrix model of, 13–14, 142–143, 143f neuropathic. See Neuropathic pain. personality factors and, 21 procedural, nonpharmacologic management of, 25 psychological aspects of, 13 psychological evaluation of, 14–20 objective personality tests in, 15, 17 screening tests in, 15 psychotherapy for, 20 radicular, 444, 447f. See also Radicular pain. referred. See Referred pain. relief of, cold therapy for, 555 spondylogenic, 314–315 Pain behavior, in biopsychosocial model of pain, 14 Pain procedures conscious sedation for, 23 planning of, 3–4 Pain rating scales, 16–17 Palpation, spinal motion, types of, 574f, 581 Palpation tests, in physical examination, 574f, 581 Paraffin bath, 553, 554f Paralysis, in multiple sclerosis, Chinese scalp acupuncture for, case report on, 184 Paraspinous block, trigger point injections with, 94 Paris approach, to manual therapy, 576–577 Patellofemoral pain syndrome (PFPS), 609 Pathologic neutral, 158 Patient, encounter with, in revenue cycle, 54 Patient catastrophizing, cognitive-behavioral therapy for, 20

Patient preparation, for selective spinal injections, 37–38 Payments, processing and analysis of, 56 Pelvic pain syndrome, chronic, acupuncture for, research on, 152 Percutaneous disc decompression, for radicular pain, 470–471 Percutaneous electrical nerve stimulation (PENS). See Percutaneous neuromodulation therapy (PNT). Percutaneous endoscopic laser annuloplasty, for radicular pain, 470 Percutaneous intradiscal radiofrequency thermocoagulation (PIRFT), for discogenic pain, 462 annular, efficacy of, 465 efficacy of, 465 intranuclear, efficacy of, 465 Percutaneous lumbar discectomy, automated, 470–471 Percutaneous neuromodulation therapy (PNT), 131 for back pain, 135–136 for bone pain, 136–137 clinical applications of, 135–138 development of, 131 electroacupuncture differentiated from, 131 mechanism of, 131–132 needle locations for, 132, 133f for neuropathic pain, 136 for post-electroconvulsive therapy headache, 137 for sciatica, 136 stimulation duration for, 133–135 stimulation montage in, 132, 134f stimulus frequency for, 132–133 technique of, 132–135 Percutaneous plasma discectomy, 470 Percutaneous radiofrequency thermomodulation, 470 Percutaneous tenotomies, 84 Peripheral neuropathy, percutaneous neuromodulation therapy for, 136 Personality Assessment Inventory (PAI), 19 Personality factors, pain therapy and, 21 Phantom limb pain, Chinese scalp acupuncture for, 179–180 case report on, 180 Phenol, 9–10 adverse reactions to, 9–10 dosage of, 9 mechanism of action of, 9 Philadelphia Panel, classification system of, for therapeutic exercises, 597, 598t Physical modalities in pain management cold, 555. See also Cold therapy. electrical stimulation as, 559. See also Electrical stimulation in pain control. manual therapy as, 573. See also Manual therapy. therapeutic exercises as, 597. See also Therapeutic exercise(s). thermal, 551. See also Thermal applications. traction as, 567. See also Traction. Physical therapy. See also Manual therapy. early, 574–575, 574f–575f Physician radiation risks to, during fluoroscopy, 35–36 radiation safety for, 31 role of, in informed consent, 57–58 training of, for selective spinal injections, 37 Physician-patient relationship, medicolegal issues and, 58–59 Pilates, 208–209, 209t Piriformis stretching long sitting, for back pain, 606, 606f posterior hip capsule stretching and, for back pain, 606, 606f–607f self-, for back pain, 606, 606f sitting, for hip pain, 613, 613f–614f supine, for back pain, 606, 606f Piriformis syndrome, 103–106 botulinum toxin injections for, 104–106, 105f–106f Piscidia erythrina (Jamaican Dogwood), for hypnotic analgesia, 188t–191t, 197

632  Index

Piscidia piscipula (Jamaican Dogwood), for hypnotic analgesia, 188t–191t, 197 Plantar fasciitis corticosteroid injections for, 86, 86f prolotherapy for, 124 Plasma rich platelet injections tendon/tendon sheath, 84 upper extremity, 64 Platelets, plasma rich, injections of tendon/tendon sheath, 84 upper extremity, 64 Pneumothorax complicating discography, 44–45 complicating intercostal nerve blocks, 45 complicating selective spinal injections, 40, 43 PNT. See Percutaneous neuromodulation therapy (PNT). Popliteal fossa sciatic nerve block, ultrasound-guided, 251–252, 251f–252f Popliteal sciatic nerve block, ultrasound-guided, 264, 264f Positional distraction cervical, 569, 570f lumbar, 571, 571f Positional palpation tests, in physical examination, 581 Positional traction, 567 Positioning, for procedure, 3 Positron emission tomography (PET), for chronic spinal pain, 538 Postoperative pain acupuncture for, research on, 151–152 massage therapy for, 212 melatonin for, 188t–191t, 198 Postprocedural care and monitoring, 28–29 Postsurgical pain, Cannabis sativa for, 188t–191t, 194 Posttraumatic stress disorder (PTSD), 223 diagnosis of, 223–225 electromagnetic dysthymia and, 224–225 mind body therapies and, 225–226 overview of, 223 symptoms of, 223 treatment protocol for, 226–227 Practice management. See Revenue cycle. Pranayama (breath control), in yoga, 205 Pratyahara (sensory inhibition), in yoga, 205 Prednisolone, 7t Prednisone, 7t Prepatellar bursitis, injections for, 80 Prilocaine, uses of, 6t Procaine, uses of, 6t Proliferants, intradiscal, for discogenic pain, 467 Prolotherapy, 113 for Achilles tendinopathy, 124 adverse events from, 126 anatomic marking and local anesthesia for, 115f, 116–126 approach to patient in, 114 in authors’ clinic, 127 clinical evidence on, 116–126 clinical recommendations for, 127 clinical vignette on, 114 contraindications to, 126 definition of, 113 for hip adductor tendinopathy, 124 for lateral epicondylosis, 121–124 for leg pain from degenerative disc disease, 125 for low back pain, 124–125 mechanism of action of, 116 nomenclature for, 113 for osteoarthritis, 125–126 patient positioning for, 114 for plantar fasciitis, 124 in practice, 126–127 professional status of, 113

Prolotherapy (Continued) for refractory coccygodynia, 125 research on contemporary, 116–126, 121f, 122t–124t early, 116, 117t–121t resources for, educational and informational, 127t for sacroiliac joint dysfunction and pain, 125 for sacroiliac joint pain efficacy of, 397 methods of, 401–402, 402f–403f side effects of, 126 Propofol, for procedural sedation, 27 Prostatitis, chronic, acupuncture for, research on, 152 Provocation discography (PD) in discogenic pain diagnosis, 461 in internal disc disruption diagnosis, 461 prerequisites for, 451, 451f Psychological aspects, of pain, 13 Psychological effects, of manual therapy, 580–581 Psychotherapy, in pain management, 20 Pterygopalatine ganglion, 513. See also Sphenopalatine ganglion. PTSD. See Posttraumatic stress disorder (PTSD). Pulmonary edema, from spinal injections, treatment of, 51 Pulse mode TENS, 561, 562t Pulsed radiofrequency (PRF) treatment, for discogenic pain, 465–466 Pumps, drug infusion, intrathecal, 494–502. See also Intrathecal drug infusion pumps, implanted. Purple coneflower (Echinacea spp.), for topical analgesia, 188t–191t, 196 Push up with ball, for shoulder pain, 616, 616f shoulder, kneel, with balance board, for shoulder pain, 616, 616f Pyogenic spondylitis, magnetic resonance imaging for, 536–537, 542f Q Quadriceps stretching, with rectus femoris stretching, for back pain, 607, 608f R RA. See Rheumatoid arthritis (RA). Rad equivalent man (rem), definition of, 31 Rad (radiation absorbed dose), definition of, 31 Radial nerve block, ultrasound-guided, 249–250, 250f Radiation effective dose equivalent of, annual individual, 33–34, 34t exposure to comparison of, by source, 35t distance and, 32–33, 33f exposure time and, 33–34, 34f factors affecting, 32–34 from imaging for chronic spinal pain, 522 occupational, National Council on Radiation Protection and Measurements recommendations for, 35t organ cancer risks from, 35t shielding and, 33 ionizing, definition of, 31 quantities and units of, 32t terminology on, 31 Radiation absorbed dose (rad), definition of, 31 Radiation safety, for physician, 31 Radicular pain, 444, 447f cervical, 444, 447f from contained disc prolapse, 451–452 definition of, 315, 441 due to contained disc prolapse, diagnosis of, 450 intradiscal chemical therapies for, 469–470 lumbar, 444 percutaneous disc decompression for, 470–471 referred pain differentiated from, 411

Index  633

Radiofrequency neurotomy. See Neurotomy, radiofrequency. Radiofrequency thermocoagulation percutaneous intradiscal, for discogenic pain, 462. See also Percutaneous intradiscal radiofrequency thermocoagulation (PIRFT), for discogenic pain. for trigeminal neuralgia, 301, 301f Radiofrequency thermoregulation lesioning, for sphenopalatine ganglion block, 514 Radiography, for chronic spinal pain, 526, 524–527, 527f–528f Radiologic procedures, 31–34 Radiosurgery, stereotactic, for trigeminal neuralgia, 302, 302f Raynaud phenomenon/disease, ginkgo for, 188t–191t, 199 Recovery, after selective spinal injections, 38 Rectus femoris stretching, with quadriceps stretching, for back pain, 607, 608f Reference pain zones, 89 Referred pain, 442–444, 443f definition of, 315 radicular pain differentiated from, 411 somatic from spinal structure, nonspecific spinal pain as, 442 zygapophysial joint pain as, 362 Reflex sympathetic dystrophy, 179 Regenerative therapies, for discogenic pain, 468–469 Relaxation for procedure, 3 for stress illnesses, 225–226 Rem (rad equivalent man), definition of, 31 Remifentanil, for analgesia, 27 Renografin (diatrizoate), 10 Residual limb pain, Chinese scalp acupuncture for, 179–180 case report on, 180 Respiratory arrest, complicating selective spinal injections, 40 Respiratory complications, of selective spinal injections, 40 Restless legs syndrome, Chinese scalp acupuncture for, 183 case report on, 183 Restructured Clinical Scales, 19 Retrocalcaneal bursitis, injections for, 80 Retroperitoneal hematomas, complicating selective spinal injections, 40 Revenue cycle accounts receivable follow-up in, 56 appointment scheduling in, 53 back-end processes in, 54t, 55–56 check-in in, 53–54 check-out in, 55 claim and statement production in, 55–56 front-end processes in, 53–55, 54t insurance verification in, 53 patient encounter in, 54 payment process and analysis in, 56 successful, implementing, 53 test/procedure coordination in, 54–55 Rheumatoid arthritis (RA) Cannabis sativa for, 188t–191t, 194 Curcuma longa for, 187, 188t–191t flare of, complicating intraarticular upper extremity injection, 64 methylsulfonylmethane for, 188t–191t, 197 omega-3 oils for, 188t–191t, 192 Tai Chi Chuan for, 215–216 vitamin D for, 188t–191t, 199 Zingiber officinalis for, 188t–191t, 193 Rhomboids stretching exercises, for neck pain, 601, 601f Rhythmic distraction, 567 Riboflavin, in pain management, 188t–191t, 197 Roentgen, definition of, 31 Rosa canina, for painful conditions, 188t–191t, 200 Rotator cuff tendinitis, corticosteroid injections for, 86

S S-adenosyl methionine (SAM-e), in pain management, 188t–191t, 197–198 Sacroiliac joint anatomy of, 391–393, 392f biomechanics of, 391–393 dysfunction of, prolotherapy for, 125 injections of. See Sacroiliac joint injections. innervation of, 392–393, 393f pain in, 391 clinical presentation of, 393–396 diagnosis of, 393–396 clinical examination in, 394–395 diagnostic injections in, 395–396 imaging in, 395 neuromodulation for, efficacy of, 397 overview of, 391 pathophysiology of, 393, 394f prolotherapy for, 125 efficacy of, 397 methods of, 401–402, 402f–403f radiofrequency neurotomy for, 396–397. See also Neurotomy, radiofrequency, for sacroiliac joint pain. surgery for, efficacy of, 397 treatment of, 396–402 efficacy of, 396–397 Sacroiliac joint injections corticosteroid, efficacy of, 396 diagnostic, 395–396 methods of, 397–399, 398f–399f St. John’s Wort (Hypericum perforatum), for analgesia, 188t–191t, 195 Saline, intradiscal, for radicular pain, 470 Salix alba (White Willow), for analgesia, 188t–191t, 196 SAM-e (S-adenosyl methionine), in pain management, 188t–191t, 197–198 Samadhi (ecstasy), in yoga, 205 Saphenous nerve anatomy of, 267, 268f entrapment of, pathophysiology and symptoms of, 267–268 Saphenous nerve block, 267 complications of, 269–270 contraindications for, 268 indications for, 268 other treatments with, 270 technique for, 269, 269f SASSI-3 (Substance Abuse Subtle Screening Inventory– Third Edition), 17 Saunders traction cervical, 570–571, 571f lumbar, 571–572, 571f Scalenes depressing clavicle exercises, for neck pain, 600, 600f Scalp acupuncture, Chinese, 173. See also Acupuncture, Chinese scalp. Scalp somatotopic system, 173–174 Scheduling, appointment, 53 Sciatic nerve anatomy of, 261, 262f injury to, complicating sciatic nerve block, 265 Sciatic nerve block, 261 anterior approach to, 262, 263f complications of, 265 fluoroscopic guided, 264–265, 265f history of, 261 indications for, 261–265 lumbar plexus, parasacral approach to, 262–263 mid-thigh, ultrasound-guided, 264 popliteal, ultrasound-guided, 264, 264f popliteal fossa, ultrasound-guided, 251–252, 251f–252f at popliteal fossa, 263, 263f

634  Index

Sciatic nerve block (Continued) posterior approach to, 261, 262f subgluteal, ultrasound-guided, 251, 251f ultrasound-guided, 264 Sciatica, percutaneous neuromodulation therapy for, 136 Scutellaria baicalensis (Huang qin), for painful conditions, 188t–191t, 200 Scutellaria laterifolia (Skullcap), for painful conditions, 188t–191t, 200 SDS (Zung Self-Rating Depression Scale), 17 Sedation conscious, 23. See also Sedation/analgesia. for discography, 420–421 for epidural steroid injections, 322 Sedation/analgesia, 23 airway assessment for, 25t antiemetics and, 25–26, 26t emergency equipment for, 26t fasting guidelines for, 24, 24t goals for, 23 Medicare guidelines for, 25 medications for, 26–28 monitoring of, 25 patient preparation and, 23–24 procedure duration/complexity and, 23, 24t provider qualifications for, 25 recovery and discharge criteria after, 28t risk classification for, 24, 24t room set-up for, 25 side effects of, 25–26 Seizures, from spinal injections, treatment of, 51 Selective spinal injections, 37 complications of, 38–42 adverse drug reactions as, 41–42 cardiovascular, 39–40 from caudal epidural injections, 42 from cervical epidural injections, 42, 44f from discography, 44–45, 45f dural puncture as, 40–41 from facet joint nerve blocks, 45 fluoroscopic exposure as, 41 infectious, 38–39 from intercostal nerve blocks, 45 from lumbar epidural injections, 42, 43f from nerve root blocks, 44 neurologic, 40 respiratory, 40 from sympathetic nerve blocks, 45 urological, 40 patient monitoring during, 45 patient preparation for, 37–38 patient recovery after, 45 physician training for, 37 Selective spinal nerve blocks, transforaminal injections versus, 333 Sensory area of cerebral cortex, acupuncture of indications for, 176 location of, 175f, 176 Sensory blocks, 240–241 Severe pain, Cannabis sativa for, 188t–191t, 194 Shielding, radiation exposure and, 33 Shingles, intercostal nerve block for, 289 Shoulder joint anterior glide of, for shoulder pain, 615, 615f dysfunction of, manual therapy for, outcomes research on, 587 external rotation of, with resistance, for shoulder pain, 615, 615f pain in acupuncture for, research on, 151 therapeutic exercises for, 614–616, 615f–616f push-ups, kneel, with balance board, for shoulder pain, 616, 616f stabilization of, for shoulder pain, 615, 615f–616f

Single photon emission computed tomography (SPECT), for chronic spinal pain, 538, 544f Sinuvertebral nerve treatments, for discogenic pain, 467 Skin preparation, for procedure, 3 Skullcap (Scutellaria laterifolia), for painful conditions, 188t–191t, 200 Sleep improvement, Cannabis sativa for, 188t–191t, 194 Soft-tissue mobilization, 578–579, 578f Solidago chilensis (Brazilian Arnica), for painful conditions, 188t–191t, 200 Somatic pain definition of, 314–315 zygapophysial joint pain as, 362 Somatic referred pain from spinal structure, nonspecific spinal pain as, 442 zygapophysial joint pain as, 362 Somatic spinal pain syndromes, definition of, 315 Somatotopic system, scalp, 173–174 Somatovisceral reflex, 164 Spasmodic torticollis, botulinum toxin injections for, 99, 100t Spasticity implanted intrathecal drug infusion pumps for, 495 neurolytic blocks for, 241 Sphenopalatine ganglion, anatomy of, 513 Sphenopalatine ganglion block, 513–514 radiofrequency thermoregulation lesioning for, 514 technique for, 513–514, 514f Spinal canal, central, stenosis of, contraindicating cervical epidural injection, 42, 44f Spinal cord infarct of, epidural steroid injection-related, 319 puncture of, epidural steroid injection-related, 318 Spinal cord stimulation, 483–494 complications of, 493–494 contraindications for, 484–485 equipment for, 485 facility for, 486 indications for, 484 percutaneous leads in placement of, 488–490, 488f–490f surgical implantation of, 490, 490f permanent laminotomy lead implantation for, 490–491, 491f pocket creation and implanted pulse generator implantation for, 491–492, 492f postoperative measures for, 492–493 preoperative considerations for, 485–486 programming in, 493 radiation safety for, 491, 491f surgical considerations for, 486 trial process considerations for, 486–488, 487f Spinal injections corticosteroids for, 8–9 selective, 37. See also Selective spinal injections. Spinal motion palpation, types of, 581, 581t Spinal nerve block, complications of, 44 Spinal pain acupuncture for, research on, 150 chronic computed tomography for, 527–530, 529f CT myelography for, 530, 530f imaging for, 521 overview of, 521 principles and strategies for, 540–541 recommendations on, early, 521–522 risk/benefit analysis of, 522–524 specificity and sensitivity considerations for, 523–524, 524t–525t magnetic resonance imaging for, 530–538 in degenerative disease, 531–536, 531f–541f in systemic disease, 536–538, 542f–544f

Index  635

Spinal pain (Continued) nuclear medicine imaging for, 538, 544f radiographs for, 524–527, 526f–528f nonspecific, 442–444 social and economic dimension of, 441 Spinal stenosis, magnetic resonance imaging for, 534–535, 539f Spine. See also Cervical spine. See also Lumbar spine. See also Thoracic spine. epidural injections for, 313. See also Epidural injections. mobility of instantaneous axes of rotation and, 359 zygapophysial joints in, 358. See also Zygapophysial joint(s) (ZJs). pain in. See Spinal pain. stability of, zygapophysial joints in, 358. See also Zygapophysial joint(s) (ZJs). zygapophysial joints of, 357. See also Zygapophysial joint(s) (ZJs). Splanchnic nerve block, 514–515 Spondylitis granulomatous, magnetic resonance imaging for, 536–537 pyogenic, magnetic resonance imaging for, 536–537 Spondylodiscitis granulomatous, magnetic resonance imaging for, 537, 543f pyogenic, magnetic resonance imaging for, 542f Spondylogenic pain, 314–315 Spondylolysis, nuclear medicine imaging for, 538, 544f Sports medicine, bromelain in, 192 Statement production, 55–56 Stellate ganglion, anatomy of, 509 Stellate ganglion block, 509–513 adequacy of, assessment of, 513 complications of, 510 contraindications for, 510 indications for, 509–510 post-injection monitoring protocol for, 513 technique for, 510–513, 512f anterior paratracheal, 510–511 lateral approach, 511–513 Stereotactic radiosurgery, for trigeminal neuralgia, 302, 302f Sternoclavicular joint, corticosteroid injections in, 67, 67f Steroids. See also Corticosteroid injections. intradiscal, for discogenic pain, 467–468 Stinging Nettles (Urtica dioica), for topical analgesia, 188t–191t, 196 Strain, vs. stress, 360 Strain counterstrain treatment, cervical region, 161–163, 163f Stress illnesses, relaxation for, 225–226 Stretching techniques, 578 Stroke, Chinese scalp acupuncture for, 180–181 case report on, 181–182 Subacromial bursitis, injections for, 77–78, 78f Subcutaneous bursitis, injections for, 80 Subdeltoid bursitis, injections for, 77–78, 78f Subgluteal sciatic nerve block, ultrasound-guided, 251, 251f Substance Abuse Subtle Screening Inventory–Third Edition (SASSI-3), 17 Subtalar joint, corticosteroid injections in, 74 Subtendinous bursitis, injections for, 80 Sufentanil, for analgesia, 27 Suffering, in biopsychosocial model of pain, 14 Superior hypogastric plexus block, 516–517 Supraclavicular nerve block, ultrasound-guided, 247, 248f Supraorbital nerve, anatomy of, 293, 294f–295f Supraorbital nerve block, 293 complications of, 295 indications for, 293–294 technique for, 294–295, 295f Supraorbital neuralgia other treatments for, 295 pathophysiology of, 293

Suprascapular nerve anatomy of, 255, 256f injury to, pathophysiology of, 255–259, 257f Suprascapular nerve block, 255 indications for, 257, 257f techniques for, 257–259, 258f–259f Swelling, reduction of, cold therapy for, 555 Sympathetic nerve blocks, complications of, 45 Sympathetic neural blockade, 507 celiac plexus block as, 514–516 complications of, 508 contraindications for, 508 ganglion impar block as, 517–518 general considerations for, 509 indications for, 507 lumbar sympathetic block as, 516f, 516 medications used for, 507 sphenopalatine ganglion block as, 513–514. See also Sphenopalatine ganglion block. splanchnic nerve block as, 514–516 stellate ganglion block as, 509–513. See also Stellate ganglion block. superior hypogastric plexus block as, 516–517 targets for, 507 uses of, 508 Sympathetically maintained/mediated pain (SMP) research on, 508 sympathetic neural blockade for, 507 Symphytum officinale (Comfrey), for topical analgesia, 188t–191t, 196 T Tachycardia, hypotension with, from spinal injections, treatment of, 51 Tai Chi Chuan, 213–216, 213f, 214t–215t for pain in ankylosing spondylitis, 216 in elderly, 216 in osteoarthritis, 215–216 of hip, 215 of knee, 215 in rheumatoid arthritis, 215–216 principles of, 213 therapeutic benefits of, evidence of, 214t–215t, 215 Tanacetum parthenium (Feverfew), for inflammation, 188t–191t, 194 Tang Gui (Angelica sinensis), for inflammation, 188t–191t, 192–193 Taut band(s) physical findings over, 89, 93f tender spots in, 89 Temporomandibular joint dysfunction of, manual therapy for, outcomes research on, 587 pain in, acupuncture for, research on, 151 Tender spots, trigger points versus, 89 Tenderness, focal, tissue injury causing, 89, 90f–92f Tendinitis biceps brachii, corticosteroid injections for, 86, 86f iliotibial band, corticosteroid injections for, 86 rotator cuff, corticosteroid injections for, 86 Tendinopathies, prolotherapy for, 121–124 Tendons/tendon sheaths anatomy and physiology of, 83, 84f corticosteroid injections of, 83–86 alternatives to, 84 complications of, 83 contraindications to, 83 efficacy of, 83 indications for, 85 lower extremity, 86, 86f methods of injection for, 84–85 side effects of, 83 upper extremity, 80f, 85–86, 85f injection of, in prolotherapy, 114

636  Index

Tennis elbow corticosteroid injections for, 85–86, 85f prolotherapy for, 121–124 Tenosynovitis, stenosing first dorsal wrist compartment, corticosteroid injections for, 85, 85f flexor, corticosteroid injections for, 85 Tenotomies, percutaneous, 84 TENS. See Transcutaneous electrical nerve stimulation (TENS). Test/procedure coordination, 54–55 Tetracaine, uses of, 6t Therapeutic exercise(s), 597 for back pain, 601–609 classification of efficacy of, 597, 598t for hip pain, 613–614, 613f–614f for knee pain, 609–611, 611f–613f for low back pain active range of motion lumbar bridging with static knee extension as, 605, 605f lumbar rotation with ball as, 606, 606f assisted hamstring stretching as, 604, 604f bridging exercises as, 605, 605f hamstring curls as, 604, 604f–605f iliopsoas self-stretching as, 607, 607f iliopsoas stretching as in side-lying position, 607, 607f in supine position, 607, 607f lumbar bridging bilateral on ball as, 605, 605f piriformis self-stretching as, 606, 606f piriformis stretching as long sitting, 606, 606f posterior hip capsule stretching and, 606, 606f–607f supine, 606, 606f resist lumbar bridging as, 605, 605f self-stretches as active range of motion, of lumbar extension prone high level, 608, 609f of erector spinae, assisted, 608, 608f lumbar stabilization as, 609, 609f of lumbar with rotation, 608, 608f of rectus femoris and quadriceps, 607, 608f for neck pain, 598–601 acute, evidence on use of, 598–599, 598t chronic, evidence on use of, 599, 599t stretching, to improve flexibility guidelines for, 600 levator scapulae stretching, 600, 600f rhomboids/trapezius stretching, 601, 601f scalenes depressing clavicle, 600, 600f trapezius stretching, 600, 600f upper trapezius stretching, 601f, 601 for shoulder pain, 614–616, 615f–616f Thermal applications, 551 clinical application of, 553 commonly used in clinical setting, 551–553 for home use, 553, 554f hot packs as, 551, 552f hydrocollator packs as, 551, 552f local, physiologic effects of, 551 paraffin bath as, 553, 554f ultrasound/ultrasonic therapy as, 551–553, 553f warm compresses as, 553, 554f Thermal intradiscal procedures (TIPs), for discogenic pain, 462 Thermocoagulation, radiofrequency percutaneous intradiscal, for discogenic pain, 462. See also Percutaneous intradiscal radiofrequency thermocoagulation (PIRFT), for discogenic pain. for trigeminal neuralgia, 301, 301f Thioctic acid, in pain management, 188t–191t, 197 Thoracic discitis, complicating discography, 44

Thoracic interlaminar epidural steroid injections, 325–328, 329f–332f Thoracic spine, 164–167 anatomy and physiology of, 164 discography of, 427–432 equipment and supplies for, 430 procedure for, 430–432, 432f–434f dysfunction of diagnosis of, 164–165 extended, treatment of, 165–166, 165f–166f flexed, treatment of, 165, 165f manual therapy for, outcomes research on, 587 epidural injections in, complications of, 43 high velocity low amplitude technique for, 163–164 in extended dysfunction, 165–166, 165f–166f in flexed dysfunction, 165, 165f loading of dynamic, 360 static, 360 transforaminal injections of, complications of, 8 zygapophysial joints of facets of, 358, 359f interventions for. See Zygapophysial joint injections. pain maps of, 363f radiofrequency neurotomy of, 383 Thoracic transforaminal epidural steroid injections, 344, 344f–347f Tibial collateral ligament (TCL) bursitis, injections for, 80, 80f Tic douloureux, 297 Tissue injury causing focal tenderness, 89, 90f–92f Topical analgesics, herbal, 188t–191t, 195–196 Torsion dystonia, botulinum toxin injections for, 99 Torticollis, spasmodic, botulinum toxin injections for, 99, 100t Traction. See also Distraction. cervical manual following inhibitive distraction, 568, 568f–569f in sitting position, 569, 569f mechanical (Saunders), 570–571, 571f over-the-door, 569–570, 570f techniques for, 568–571 clinical studies on, 567–568 definition of, 567 lumbar mechanical (Saunders), 571–572, 571f techniques of, 571–572 manual, sustained or intermittent, 567 mechanical, sustained or intermittent, 567 positional, 567 spinal contraindications for, 568 indications for, 568 therapeutic effects of, 567–568 therapeutic efficacy of, treatment adjuncts to increase, 572 Transcutaneous electrical nerve stimulation (TENS) acupuncture mode, 561, 562t burst or pulse mode, 561, 562t conventional mode, 561, 562t indications and contraindications for, 564t modulated mode, 562, 562t in pain control acupuncture theory of, 561 clinical use and application of, 561, 562t efficacy of, evidence of, 564–565 electrode placement for, 561 endorphin theory of, 561, 561f gate control theory of, 560, 560f practical application of, 561–562 proposed mechanisms of, 560–561 Transducers, for nerve blocks, 243–245, 245f Transduction, in zygapophysial joint pain, 360

Index  637

Transforaminal injections cervical, complications of, 8 lumbar, complications of, 8 thoracic, complications of, 8 Transforaminal technique, for epidural steroid injections cervical, 344–348, 347f–350f sample dictation for, 351 lumbar, 335–344, 341f–343f S1, 333–335, 338f–340f thoracic, 344, 344f–347f Trapezius stretching exercises for neck pain, 600–601, 600f–601f upper, for neck pain, 601, 601f Triamcinolone acetonide (Kenalog), 8 Triamcinolone (Aristocort, Kenalog), 7t, 8 adverse reactions to, 41 Triamcinolone diacetate (Aristocort Forte), 8 Triamcinolone hexacetonide (Aristospan), 8 Trigeminal nerve, anatomy of, 297, 298f Trigeminal neuralgia cryotherapy for, 301 decompressive procedures for, 302–303, 303f diagnosis of, 298–299, 298t gasserian ganglion techniques for, 301–302, 301f head and facial, 297 interventional approaches to, 299–303 medical treatment of, 299 microvascular decompression for, 302–303, 303f neurectomy for, 300–301 neurostimulation for, 303 peripheral nerve blocks for, 299 of mandibular nerve and its branches, 300 with local anesthetics and streptomycin, 300 of maxillary nerve and its branches, 300, 300f neurolytic, 301 of ophthalmic nerve, 299–300, 300f stereotactic radiosurgery for, 302, 302f Trigger point injections, 89 block before, 94 care after, 94 contraindications for, 90 effectiveness of, 90 for myofascial pain syndrome, botulinum toxin injections versus, 101 with needling, physical findings before, during and after, 89, 93f, 93t procedure for, 92–94 techniques of, 90–92 corticosteroid injections as, 91 of J. Travell and D.G. Simons, 91 needling with infiltration of taut band as, 90–91 Trigger points biochemical milieu of, 144 definition of, 89 physical findings over, 89, 93f tender spots versus, 89 Trigger thumb/digit, corticosteroid injections for, 85 Trochanteric bursitis, injections for, 78–79, 79f Tunneling damage, complicating spinal cord stimulation, 494 Turmeric (Curcuma longa), for inflammation, 187–192, 188t–191t U Ulnar nerve block, ultrasound-guided, 249, 250f Ultrasound-guided nerve blocks, 243 axillary, 248–249, 249f brief facts on, 243–246 femoral, 250–251, 251f iliohypogastric, 286, 287f ilioinguinal, 286, 287f infraclavicular, 247–248, 248f–249f

Ultrasound-guided nerve blocks (Continued) interscalene, 246, 247f lateral femoral cutaneous, 276–277, 277f lower extremity, 250–252 median, 249, 249f–250f nerve stimulator in, 246 overview of, 243 popliteal fossa sciatic, 251–252, 251f–252f preparing for, 246 radial, 249–250, 250f sciatic, 264 mid-thigh, 264 popliteal, 264, 264f subgluteal sciatic, 251, 251f supraclavicular, 247, 248f suprascapular, 258, 258f ulnar, 249, 250f upper extremity, 246–250 Ultrasound therapy, 551–553, 553f Upper extremity joint injections in, 63. See also Intraarticular injections, of corticosteroids, in upper extremity. nerve blocks in, ultrasound-guided, 246–250 tendon/tendon sheath injections in, 85–86 Urological complications, of selective spinal injections, 40 Urtica dioica (Stinging Nettles), for topical analgesia, 188t–191t, 196 Urticaria from medications, treatment of, 11 from spinal injections, treatment of, 51 V Vagal reaction, from spinal injections, treatment of, 51 Valerian (Valeriana officianalis), for hypnotic analgesia, 188t–191t, 197 Valeriana officianalis (Valerian), for hypnotic analgesia, 188t–191t, 197 Valium (diazepam), in conscious sedation, 26 Vapocoolant sprays, 558 VAS (Visual Analog Scale), for rating pain, 16 Vascular injury, complicating sciatic nerve block, 265 Vasovagal reactions, to medications, treatment of, 11 Vasovagal responses, to epidural injections, 316 Venous insufficiency, Centella asiatica for, 200 Versed (midazolam), in conscious sedation, 26 Vertebral osteomyelitis, complicating selective spinal injections, 39f Vertigo, in multiple sclerosis, Chinese scalp acupuncture for, case report on, 184–185 Viburnum opulus (Cramp Bark), for painful conditions, 188t–191t, 200 Viburnum prunifolium (Black Haw), for painful conditions, 188t–191t, 200 Visceral pain, definition of, 314–315 Viscerosomatic reflex, 164 Viscosupplementation, 10 intraarticular, in upper extremity, 64 Visual Analog Scale (VAS), for rating pain, 16 Vitamin D, for painful conditions, 198–199 W Warm compresses, 553, 554f White Bryony (Bryonia alba), for analgesia, 188t–191t, 195 White Willow (Salix alba), for analgesia, 188t–191t, 196 Wong-Baker FACES Pain Rating Scale, 16 Wound dehiscence complicating implanted intrathecal drug infusion pumps, 499 complicating spinal cord stimulation, 493, 494f Wound healing, bromelain in, 188t–191t, 192 Wrist corticosteroid injections in, 68, 68f–69f dysfunction of, manual therapy for, outcomes research on, 588

638  Index

X X-rays, definition of, 31 Y Yama (moral and ethical behavior), in yoga, 205 Yanhusuo (Corydalis yanhusuo), for analgesia, 188t–191t, 194 Yoga, 205–208 benefits of, on pain in cancer, 208 in carpal tunnel syndrome, 207 chronic, 206–207, 208t chronic back, 206, 208f chronic low back, 205–206, 207t in fibromyalgia, 206 in migraine, 207 in osteoarthritis, 207–208 of knee, 206 elements of, 205, 213 Z Zingiber officinalis (Ginger), for inflammation, 188t–191t, 193 ZJs. See Zygapophysial joint(s) (ZJs). Zung Self-Rating Depression Scale (SDS), 17 Zygapophysial joint(s) (ZJs) anatomy of, 357–360, 358f biomechanics of, 357–358, 359f osteoarthritis of, magnetic resonance imaging for, 535–536, 540f–541f pain in, 357, 360–362 cervical, referral patterns of, 443–444, 444f diagnosis of, 362–385 epidemiology of, 362 etiology of, 360–361 interventions for. See Zygapophysial joint injections. mechanisms of, 360 pathology of, 361, 361f–362f treatment of, 379–385 development of, 379–380 intraarticular corticosteroid injections in, 380–381, 380f–381f radiofrequency neurotomy in. See Zygapophysial joint(s) (ZJs), radiofrequency neurotomy of.

Zygapophysial joint(s) (Continued) radiofrequency neurotomy of cervical development of, 381 effectiveness of, 382–383 procedure for, 381–382, 382f lumbar effectiveness of, 383–385 procedure for, 383, 383f thoracic, 383 Zygapophysial joint injections contraindications for, 366 diagnostic intraarticular blocks as, 376–379 atlantooccipital joint, 378–379, 379f development of, 376–377 lateral atlantoaxial joint interpretation of results of, 377 procedure for, 377, 378f–379f validity of, 377–378 indications for, 365–366 medial branch blocks as, 366–376 cervical C7, procedure for, 371, 371f C3 to C6 interpretation of results of, 370–371 procedure for, 366–370, 367f–370f third occipital, procedure for, 371–372, 372f–373f validity of, 372–373 development of, 366 lumbar interpretation of results of, 376 procedure for, 375–376, 375f–376f validity of, 376 thoracic interpretation of results of, 374 procedure for, 374, 374f–375f validity of, 375 risks of, 366